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        <title>Frontiers in Cell and Developmental Biology | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/cell-and-developmental-biology</link>
        <description>RSS Feed for Frontiers in Cell and Developmental Biology | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-14T11:13:37.734+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1764767</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1764767</link>
        <title><![CDATA[Association of baPWV and CD34+ progenitor-derived exosomal hsa_circ_0093884 with Alzheimer’s disease: mechanistic insights into the miR-375/SIX4 axis]]></title>
        <pubdate>2026-05-14T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ying Chen</author><author>Yangyang Huang</author><author>Bei Gao</author><author>Yuhao Zhao</author><author>Lu Wei</author><author>Guoxin Ye</author><author>Shuyan Chen</author><author>Xibao Shi</author><author>Ruiliang Wang</author><author>Fei Wang</author>
        <description><![CDATA[BackgroundVascular aging plays a key role in the pathogenesis of Alzheimer’s disease (AD). This study evaluated the diagnostic value of arterial stiffness and endothelial progenitor CD34+ progenitor-derived exosomal circRNAs (EPC-Exos circRNAs) in AD, and examined their associations with Comprehensive Geriatric Assessment (CGA) measures.MethodsWe measured brachial-ankle pulse wave velocity (baPWV) and conducted CGA in subjects with AD (n = 58), mild cognitive impairment (MCI, n = 31), and non-cognitive impairment (NCI, n = 36). Plasma levels of SIRT1-derived circRNAs (including hsa_circ_0093884) within EPC-Exos were quantified. Logistic regression and ROC curve analyses were used to assess diagnostic performance, with internal validation performed using bootstrapping (1,000 resamplings) to evaluate model stability. Aβ1-42-treated SH-SY5Y cells were used as a neuronal model to validate the downstream neuroprotective effects of circRNA. The miR-375/SIX4 regulatory axis was investigated using bioinformatics prediction, biotin-RNA pull-down, dual-luciferase reporter assays, and co-transfection experiments.ResultsCompared to MCI and NCI groups, AD patients exhibited significantly higher baPWV and lower levels of EPC-Exosomal hsa_circ_0093884 (P < 0.01). A composite model incorporating baPWV, hsa_circ_0093884, and CGA scores showed excellent diagnostic performance (AUC = 0.943; 95% CI: 0.881–1.000), with the robustness of key predictors confirmed by bootstrap validation. In Aβ1-42-treated SH-SY5Y cells, overexpression of hsa_circ_0093884 increased cell viability and reduced apoptosis, whereas knockdown further decreased viability and promoted apoptosis. Mechanistically, hsa_circ_0093884 directly interacted with miR-375 and regulated SIX4 expression.ConclusionEPC-Exosomal hsa_circ_0093884 and baPWV are valuable diagnostic biomarkers associated with Alzheimer’s disease. The hsa_circ_0093884/miR-375/SIX4 axis offers a novel therapeutic target, supporting a potential vascular-neuronal axis connecting vascular aging to neurodegeneration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1804251</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1804251</link>
        <title><![CDATA[Genomic and proteomic conversion of brain ischemia to Alzheimer’s disease]]></title>
        <pubdate>2026-05-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Ryszard Pluta</author><author>Marzena Ułamek-Kozioł</author>
        <description><![CDATA[Despite many years of extensive research into the etiology and treatment of Alzheimer’s disease, based on the importance of amyloid and tau protein as causative factors, these studies have stalled, have not brought any breakthroughs and, most importantly, have not led to any final conclusions. Therefore, the ineffectiveness of the above-mentioned actions and the pressure from the community of people affected by Alzheimer’s disease forced the scientific community to change its way of thinking about the etiopathogenesis of this disease. This situation has prompted a group of scientists who have been studying the effects of brain ischemia for years to focus on post-ischemic changes, which–similarly to Alzheimer’s disease–predominate in the hippocampus, leading to the development of amyloid plaques, neurofibrillary tangles and ultimately to dementia. In this context, it has been proposed that brain ischemia may play an important role in driving amyloid and tau protein pathology in the development of Alzheimer’s disease. In this review, we present an update of extensive experimental and clinical studies conducted over several years on the role of brain ischemia in the neuropathogenesis of Alzheimer’s disease. Current advances in understanding the ischemic etiology of Alzheimer’s disease have revealed dysregulation of Alzheimer’s disease-associated genes, including secretases, amyloid precursor protein, apoptosis, autophagy, mitophagy, tau protein, α-synuclein, apolipoproteins, LRP1, and RAGE. This article presents the relationship between genes which dysregulation is a result of brain ischemia and the cellular and tissue neuropathology characteristic of Alzheimer’s disease and their proteins. These observations clearly indicate that, following brain ischemia, changes occur in the expression of Alzheimer’s disease-associated genes and in the folding of disease-associated proteins such as amyloid, tau protein, and α-synuclein. This leads to massive neuronal death and disruption of the neuronal network, ultimately leading to the development of Alzheimer’s disease-like dementia. Data indicate common genomic and proteomic factors in brain ischemia and Alzheimer’s disease. It seems that the brain ischemia model may be useful in determining the role of folding proteins and their genes dysregulation in Alzheimer’s disease. In the future, manipulation of genes and proteins associated with ischemia and ischemia-induced Alzheimer’s disease will likely provide new hope for developing causal therapies that are urgently needed to prevent or treat Alzheimer’s disease. The innovative/novel approach to the etiology of Alzheimer’s disease presented in this review will provide stakeholders with a glimpse into the future.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1827716</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1827716</link>
        <title><![CDATA[T cell exhaustion landscapes and therapeutic modulation in cancer immunity]]></title>
        <pubdate>2026-05-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jhommara Bautista</author><author>Andrés López-Cortés</author>
        <description><![CDATA[T cell exhaustion is a central framework for explaining why antitumor T cell responses often fail despite persistent antigen exposure and immune infiltration. Rather than a single dysfunctional endpoint, exhaustion is increasingly understood as a structured and dynamic continuum of antigen-experienced CD8+ T cell states that differ in proliferative capacity, effector potential, epigenetic constraint, metabolic fitness, and spatial distribution within tumors. This view has major therapeutic implications because clinically relevant interventions can remodel exhausted-state composition and function without fully restoring a non-exhausted identity. In this review, we examine the organization of exhausted T cell states from progenitor-like to terminal compartments and discuss how TOX-linked survival programs, epigenetic fixation, and tumor-imposed metabolic and spatial constraints stabilize exhausted fate under chronic stimulation. We highlight the role of progenitor exhausted T cells in sustaining therapeutic responsiveness, explain why reinvigoration after checkpoint blockade is often partial rather than transformative, and evaluate emerging strategies to modulate exhaustion dynamics, including combination immunotherapy and engineered control systems in CAR T cells. Together, these concepts support a shift from viewing exhaustion as a binary defect to understanding it as a constrained state system that can be measured, preserved, and selectively redirected. Defining which exhausted states remain productively controllable, and under what conditions, will be essential for developing more durable and mechanistically informed cancer immunotherapies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1804813</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1804813</link>
        <title><![CDATA[Mitophagy in inflammatory bowel disease: regulatory mechanisms and therapeutic potential]]></title>
        <pubdate>2026-05-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Sixuan Chen</author><author>Jing Guan</author><author>Xia Pang</author><author>Xi Chen</author><author>Min Li</author><author>Huan Wang</author><author>Fei Mao</author>
        <description><![CDATA[Inflammatory bowel disease (IBD), encompassing Crohn’s disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder of the gastrointestinal tract driven by complex interactions among genetic susceptibility, barrier dysfunction, and immune dysregulation. Mitophagy, the selective autophagic clearance of damaged mitochondria, has emerged as a key regulator of intestinal homeostasis and immune balance. Impaired mitophagy compromises epithelial barrier integrity, amplifies inflammatory signaling, and promotes disease progression. This review summarizes the molecular mechanisms of mitophagy, examines its involvement in IBD pathogenesis across intestinal epithelial and immune cell compartments, and highlights mitophagy-modulating compounds that may inform the development of novel therapeutic strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1811727</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1811727</link>
        <title><![CDATA[The emerging roles of microRNAs in pneumoconiosis: pathogenic mechanisms and clinical implications]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xuanyan He</author><author>Lanxi Ye</author><author>Guangchao Zhou</author><author>Xia Li</author>
        <description><![CDATA[Pneumoconiosis is currently one of the most common occupational diseases in clinical practice. Its pathogenesis has not yet been fully elucidated, and effective clinical treatments are lacking. MicroRNAs (miRNAs) are a class of non-coding single-stranded RNA molecules that regulate gene expression at the post-transcriptional level by binding to target genes, thereby inhibiting mRNA translation or promoting mRNA degradation. Existing studies have shown that miRNAs are closely associated with the development and progression of pneumoconiosis, making them important candidate biomarkers for early screening and diagnosis of the disease. This review summarizes the current research status and advances regarding miRNAs in pneumoconiosis, aiming to provide new insights and approaches for understanding its pathogenesis, as well as for early warning, diagnosis, and treatment.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1802828</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1802828</link>
        <title><![CDATA[Mesenchymal stem cell and exosome-based therapies for degenerative disc disease: from mechanisms to clinical translation]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Baoliang Li</author><author>Yanyan Zhang</author><author>Changjiao Ji</author><author>Zhigang Shi</author><author>Nianhu Li</author>
        <description><![CDATA[Degenerative disc disease (DDD) is a leading cause of chronic low back pain and disability worldwide, placing a significant burden on public health systems and economies. The pathogenesis of DDD is characterized by oxidative stress, chronic inflammation, dysregulated cell death, and impaired extracellular matrix (ECM) homeostasis, all of which contribute to the structural degradation and functional impairment of intervertebral discs. Current clinical treatments primarily offer palliative relief, underscoring the urgent need for regenerative therapies that address the underlying pathological mechanisms. Mesenchymal stem cells (MSCs) and their exosomes (Exos) have emerged as promising candidates for DDD therapy, as they stimulate ECM synthesis, regulate inflammation, and enhance cell survival. Furthermore, advanced biomaterials have been developed to create bioactive environments that enhance cell retention and facilitate controlled therapeutic delivery. This review provides a comprehensive overview of the molecular mechanisms driving DDD, evaluates MSC/Exo and biomaterial-based therapies, and explores emerging technologies for personalized treatment strategies aimed at restoring disc function, extending beyond symptomatic management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1791121</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1791121</link>
        <title><![CDATA[Phenotypic transformation of HCC827 cells revealed by evaluation of human platelet lysate as a sustainable fetal bovine serum replacement]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Clemens Woitaske-Proske</author><author>Niklas Keller</author><author>Louisa Zinke</author><author>Dennis Schade</author><author>Christian Peifer</author>
        <description><![CDATA[Fetal bovine serum (FBS), a widely used supplement in cell culture, raises ethical and scientific concerns due to its animal origin, batch variability, and limited physiological relevance for human cells. As part of our efforts to adopt more sustainable and human-relevant cell culture conditions, we investigated human platelet lysate (HPL) as an alternative to FBS for culturing non-small cell lung carcinoma (NSCLC) cells. Different compositions of both sera were assessed by ELISA, showing comparable FGF2 content but 2-fold higher amount of TGF-β1 in HPL compared to FBS. Notably, when cultured with HPL, HCC827 cells developed distinct phenotypes, including ring-like f-actin structures, increased spheroid roundness and size. Canonical endothelial-to-mesenchymal transition (EMT) was not detected, supported by Western blot analysis of key markers Vimentin and SNAI1. Instead, a hybrid EMT signaling state based on kinome activity profiling data is visible but cannot fully explain the visible phenotypical changes. Furthermore, kinome activity profiling at different timings revealed significant HPL-dependent changes for HCC827 cells pointing at altered integrin signaling, distinct from those observed in the other NSCLC lines A549 and H1299. Our findings highlight the cell-type-specific effects of HPL compared to FBS and underscore the importance of case-by-case evaluation when considering HPL as an alternative to FBS in cellular models.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1752740</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1752740</link>
        <title><![CDATA[Defining the urine proteome in boys with posterior urethral valves: a pilot study]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xin Wang</author><author>Hanna Cortado</author><author>Liwen Zhang</author><author>Christina B. Ching</author><author>Ashley R. Jackson</author><author>John W. Froehlich</author><author>Richard S. Lee</author><author>Brian Becknell</author><author>Daryl McLeod</author>
        <description><![CDATA[IntroductionPosterior urethral valves (PUV) is the most common cause of congenital bladder outlet obstruction and a major etiology of end-stage kidney disease in boys. There are significant knowledge gaps about the pathogenesis and prognostic indicators of kidney and bladder dysfunction in boys with PUV.MethodsWe utilized liquid chromatography-tandem mass spectrometry to analyze the urine proteome in a pilot cohort of 20 boys with PUV compared to 20 unaffected controls, with a focus on estimated glomerular filtration rate (eGFR) variation within the PUV group and its impact on urine protein signatures. Eight complementary workflows for differential expression analysis were developed to ensure robust detection of differential protein expression. A single-cell RNA-seq atlas of 162,083 healthy kidney, ureter, and bladder cells was assembled to infer tissue and cellular origins of PUV-associated proteins.ResultsIn cases of PUV with preserved eGFR, upregulation of keratins and uroplakins was detected, suggestive of urothelial injury and remodeling that may reflect bladder dysfunction that occurs early in the disease process, even before a decline in renal function. In contrast, cases with low eGFR were associated with declining levels of the proteins related to viability and synthetic function of specific nephron and collecting duct segments, along with increased levels of proteins related to complement activation and inflammation, suggestive of progressive renal injury. The single-cell atlas provided biological context, identifying putative renal and urothelial cell sources for these proteins.ConclusionThis integrative analysis highlights biological pathways and proteins that may reflect kidney and urinary tract injury and dysfunction in a pilot cohort of boys with PUV. These initial findings warrant further testing in longitudinal studies with larger cohorts to link the urine proteome to clinically relevant kidney and bladder outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1818014</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1818014</link>
        <title><![CDATA[TRIM family proteins: dual roles in tumor immunity]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Runjie Cai</author><author>Liang Chen</author>
        <description><![CDATA[Tripartite motif (TRIM) proteins represent one of the largest subfamilies of E3 ubiquitin ligases and exert complex yet critical dual roles in tumor immunology by orchestrating protein ubiquitination. This review systematically delineates the multifaceted regulatory roles of TRIM proteins in tumor immunity, with a focus on their dual functions within the tumor immune microenvironment, particularly regarding immune checkpoints and tumor-infiltrating immune cells. Notably, the same TRIM protein may exert opposing immunomodulatory effects in different tumor types or microenvironmental contexts, underscoring the critical influence of context on their functions. This article aims to synthesize current advances in understanding the dual roles of the TRIM family in tumor immunity and to discuss their potential and challenges as novel targets for immunotherapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1811421</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1811421</link>
        <title><![CDATA[p300: expanding beyond acetylation to mastermind lactylation-dependent tumorigenesis]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Su-Ting Jiang</author><author>Xiao He</author><author>You-Wei Wang</author><author>Wan-Song Chen</author><author>Peng Guan</author>
        <description><![CDATA[The transcription coactivator p300 is canonically recognized as a histone acetyltransferase that orchestrates chromatin remodeling and gene expression. However, recent breakthroughs have expanded the catalytic landscape of p300 beyond acetylation to include lactylation, a metabolic stress induced modification driven by lactate accumulation. As a principal lactyl-transferase, p300 acts as a sensor of the Warburg effect, directly translating cellular metabolic status into epigenetic regulation. This catalytic duality extends beyond histones to non-histone substrates, profoundly impacting tumor progression, immune evasion, and metabolic adaptation. This review synthesizes the established roles of p300 in acetylation while critically examining its emerging identity as a writer of protein lactylation. By highlighting the competitive interplay between acetyl-CoA and lactyl-CoA usage, we position p300 as a central integrator that couples metabolic signaling with transcriptional reprogramming in cancer and other pathological states. Furthermore, this review bridges the gap between mechanistic discovery and clinical translation by evaluating the therapeutic potential of targeting p300 lactyl-transferase activity. We highlight the emerging clinical relevance of p300 inhibitors, such as CCS1477 (in Phase I/II trials) and the preclinical agent A-485, discussing how these compounds, originally designed for acetylation or bromodomain inhibition, may be repurposed to dismantle lactylation-driven oncogenic networks and overcome metabolic immune evasion in refractory tumors.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1837383</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1837383</link>
        <title><![CDATA[Cell type–specific paradox of autophagy and senescence in MASH: implications for precision hepatology]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Md Entaz Bahar</author><author>Deok Ryong Kim</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1807454</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1807454</link>
        <title><![CDATA[HMGB1 regulates mitochondrial structure and reactive oxygen species balance during the transition from naïve to primed pluripotency]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tatiana Y. Starkova</author><author>Sergey V. Ponomartsev</author><author>Veniamin S. Fishman</author><author>Nariman R. Battulin</author><author>Nikolay D. Aksenov</author><author>Evgeny I. Bakhmet</author><author>Andrey A. Kuzmin</author><author>Dmitry S. Bogolyubov</author><author>Sergey A. Sinenko</author><author>Alexey N. Tomilin</author>
        <description><![CDATA[IntroductionEmbryo implantation is characterized by the process of naïve-to-primed pluripotency transition in epiblast cells, involving an anabolic boost, mitochondrial remodeling, and increased proliferation. Yet, the molecular mechanisms underlying these extensive changes remain poorly understood. High mobility group box 1 (HMGB1) is a non-histone, redox-sensitive chromatin protein involved in diverse cellular processes, however its role in pluripotency control has not been fully characterized.MethodsTo determine the function of HMGB1 in mouse embryonic stem cells (ESCs), Hmgb1-knockout (KO) ESCs were generated using CRISPR/Cas9 system. KO ESCs were analyzed for cell proliferation, cell cycle progression, and apoptosis, as well as for levels of active mitochondria, mitochondrial membrane potential, and reactive oxygen species (ROS) using fluorescent-based reagents and flow cytometry. Pluripotency was assessed by analyzing the expression of pluripotency markers with immunocytochemistry, Western blotting, qRT-PCR, as well as by teratoma formation assay. Naïve-to-primed pluripotency transition was investigated by in vitro culture. Molecular analysis was performed with RNA sequencing, bioinformatics, qRT-PCR, and Western blotting. The ultrastructure of mitochondria was examined using transmission electron microscopy.ResultsWe first successfully generated HMGB1 KO in mouse ESCs and showed that HMGB1 function is dispensable for both cell viability and pluripotency maintenance, while it is required for the cell proliferation boost during the naïve-to-primed pluripotency transition. Molecular and transcriptomic analysis identified the involvement of HMGB1 in the regulation of energy metabolism processes by regulating mitochondrial structure and function, as well as ROS homeostasis. Loss of HMGB1 function in mouse ESCs results in altered mitochondrial structure and excessive ROS production. HMGB1-dependent elevated ROS levels negatively regulate cell proliferation during the transition from naïve to primed pluripotency in vitro.ConclusionWhile HMGB1 deficiency does not impair self-renewal in the naïve state, it causes a marked reduction in proliferation as cells advance to primed pluripotency. Our findings thus identify HMGB1 as a key regulator of mitochondrial integrity and ROS homeostasis during the naïve-to-primed pluripotency transition.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1830798</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1830798</link>
        <title><![CDATA[Endometrial organoid and stromal cultures demonstrate donor-derived cellular origin of the endometrium after uterus transplantation]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lisa M. Meisl</author><author>Ingrid A. Teufel</author><author>Anjali Ralhan Singh</author><author>Annette Staebler</author><author>Melanie Henes</author><author>Sara Y. Brucker</author><author>Katharina Rall</author><author>André Koch</author>
        <description><![CDATA[The human endometrium undergoes cyclical regeneration during the menstrual cycle, a process thought to be driven primarily by multipotent stem cells located within the basalis layer. Previous studies have proposed that bone marrow–derived cells (BMDCs) may contribute to endometrial regeneration; however, this hypothesis remains controversial due to methodological limitations in distinguishing hematopoietic cells from resident endometrial epithelial or stromal populations. To investigate the potential contribution of BMDCs to endometrial regeneration, we used uterus transplantation (UTx) as a unique donor–recipient model and established patient-derived 3D endometrial organoid (PDO) and 2D stromal cell cultures from UTx recipients. These culture systems enable selective expansion of epithelial and stromal compartments while excluding hematopoietic cells, thereby allowing accurate assessment of cellular origin through donor–recipient genotyping. Samples were collected from four UTx cases spanning up to 7 years, including biopsies obtained before and after pregnancy as well as tissue collected at uterus explantation. Short tandem repeat (STR) profiling was performed on genomic DNA isolated from donor and recipient blood, endometrial organoids, and stromal cell cultures to determine cellular genotype. Endometrial epithelial organoids derived from all UTx cases exhibited consistent morphological features comparable to healthy endometrium and demonstrated long-term expandability. STR analysis revealed complete concordance between the donor genotype and both epithelial and stromal cells of the transplanted uteri, with no evidence of recipient-derived cells or BMDC contribution to the endometrium. These findings indicate that the cellular composition of the endometrium in transplanted uteri remains donor-derived over extended follow-up, including after pregnancy. Together, these results provide strong evidence against a substantial contribution of BMDCs to endometrial regeneration and establish patient-derived endometrial organoid and stromal cultures as powerful model systems for investigating endometrial biology and regenerative mechanisms.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1830777</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1830777</link>
        <title><![CDATA[Monocytes and neutrophils promote cardiac fibroblast pro-fibrotic phenotypes through IL-6 and MIF]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zhongxiao Cong</author><author>Aleksandar Ivetic</author><author>Maddy Parsons</author>
        <description><![CDATA[Cardiac fibrosis, characterized by activation of cardiac fibroblasts and accumulation of extracellular matrix (ECM), is associated with most cardiac pathological conditions, leading to adverse cardiac remodeling and accelerating progression of heart failure. Immune cell recruitment is a hallmark of early fibrosis; however, the underlying mechanisms linking early inflammation, fibroblast activation and perpetuation of cardiac fibrosis remain unclear. In this study, cell-derived matrices (CDM) and collagen gels were used to investigate primary human cardiac fibroblast (HCF) pro-fibrotic response, native ECM synthesis and interactions with immune cells. Direct co-culture of HCF with THP-1 and HL-60 cells, or conditioned media from HCF-immune cell co-cultures, resulted in enhanced HCF-induced contraction of collagen gels - a finding recapitulated using primary human monocytes and neutrophils. Pro-fibrotic cytokines, macrophage migration inhibitory factor (MIF) and interleukin-6 (IL-6), were upregulated in HCF-immune co-cultures and were further confirmed as active regulators of HCF contraction using recombinant purified cytokines and function blocking antibodies. Live imaging revealed that THP-1 cells increased HCF migration, which was suppressed by an IL-6 neutralizing antibody. These findings provide insight into the effects of early exposure of HCF to immune cells and shed light on early pro-fibrotic initiation mechanisms and therapeutic targets.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1788958</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1788958</link>
        <title><![CDATA[3D Ultrastructural segmentation of human microvasculature reveals new insights in pericyte-endothelial cell interactions]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Timothy E. Vanderleest</author><author>Joseph F. Arboleda-Velasquez</author>
        <description><![CDATA[IntroductionCapillary structure remains incompletely characterized at the nanoscale level. Advances in 3D electron microscopy datasets provide new opportunities to systematically examine microvascular architecture and cellular interactions.MethodsWe performed 3D image segmentation of human cerebral cortex microvasculature using the publicly available H01 Release dataset. This initial analysis focused on descriptive and quantitative characterization of the basement membrane, peg-and-socket cell interactions, and other subcellular features.ResultsWe identified several novel structural features. In addition to known bidirectional peg-and-socket connections between pericytes (PCs) and endothelial cells (ECs), we observed similar structures between neighboring ECs and at interfaces where ECs form junctions with themselves. PC pegs showed an unexpected preference for proximity to EC nuclei and were enriched at PC edges. The PC endoplasmic reticulum (ER) frequently contacted the plasma membrane on the lumen-facing surface, particularly at sites corresponding to sockets of EC pegs. We also identified electron-lucent pockets (ELPs) at interfaces between ECs and PCs, as well as within the basement membrane.DiscussionThese findings expand current understanding of capillary ultrastructure by revealing previously unrecognized interactions between vascular cells and novel subcellular features. The observed structural features may have functional implications for signaling, stability, and vascular mechanics, warranting further investigation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1859260</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1859260</link>
        <title><![CDATA[Editorial: Molecular mechanisms and therapeutic strategies of head and neck disease]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Yu-Jing Song</author><author>Xu Zhang</author><author>Jian-Hua Wang</author><author>Wei-Wei Deng</author><author>Lei-Lei Yang</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1849677</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1849677</link>
        <title><![CDATA[Correction: Immunosenescence and metabolic reprogramming in MASLD: an age-dependent immunometabolic vicious cycle and therapeutic opportunities]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Yuxin Xu</author><author>Qiuxiang Li</author><author>Xuehua Jiao</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1830394</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1830394</link>
        <title><![CDATA[Mast cell driven immunometabolism as a therapeutic entry point in ESCC]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Zhifeng Qu</author><author>Xuewei Zheng</author><author>Anshun Zhao</author><author>Pei Wang</author><author>Shegan Gao</author><author>Qinan Yin</author>
        <description><![CDATA[Esophageal squamous cell carcinoma (ESCC) remains one of the most aggressive epithelial malignancies, with most patients deriving only modest benefit from surgery, chemoradiotherapy, or immune checkpoint inhibition. Recent studies suggest that tumor metabolic reprogramming and immune dysfunction evolve together and reinforce one another, yet the causal links between these processes remain only partially understood. Mast cells (MCs) represent a stromal population that has received more attention. Although associated with allergic reactions, tissue repair, and inflammatory responses under normal physiology, MCs in ESCC frequently occupy stromal, vascular and hypoxic zones where metabolic stress is most pronounced. This spatial distribution suggests that MCs actively shape tumor metabolic states through the release of lipid mediators, including prostaglandins, leukotrienes, and platelet activating factor (PAF). These mediators amplify lipid metabolic programs in tumor cells and contribute to an immunosuppressive environment in which dendritic cell priming is attenuated, and cytotoxic T cell (CTL) function is progressively impaired. MC-derived cytokines and proteases further remodel the extracellular matrix and reorganize stromal architecture, collectively facilitating the invasion of malignant cells into adjacent tissue. Single cell and spatial transcriptomic analyses have revealed substantial heterogeneity among tumor-infiltrating MCs, indicating that distinct phenotypic subsets engage divergent metabolic and immune circuits and that only a subset may be functionally tumor permissive. These findings have generated increasing interest in therapeutic strategies targeting MC-linked mediators, inhibiting lipid metabolic enzymes, or integrating metabolic modulation with immune checkpoint therapy. A rigorous mechanistic understanding of how MCs coordinate metabolic and immune remodeling in ESCC may ultimately support biomarker-guided patient stratification and inform novel therapeutic combinations capable of overcoming resistance to current treatment modalities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1813995</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1813995</link>
        <title><![CDATA[Epigenetic dysregulation in mycosis fungoides and sézary syndrome]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Vinícius de Camargo Callefi</author><author>Isadora Alves</author><author>Nélio Cézar De Aquino</author><author>Sofia Cattena</author><author>Emanuelle Santos</author><author>Ketelyn Vasconcelos</author><author>Hebert Fabricio Culler</author><author>Luís Alberto de Pádua Covas Lage</author><author>Vanderson Rocha</author><author>Adriana Castello Costa Girardi</author><author>José Antonio Sanches</author><author>Carlos Alejandro Murga-Zamalloa</author><author>Juliana Pereira</author><author>Cadiele Oliana Reichert</author>
        <description><![CDATA[Cutaneous T-cell lymphomas (CTCL), including mycosis fungoides (MF) and Sézary syndrome (SS), remain challenging to diagnose at early stages and to manage durably. Although staging and classification have improved, early MF can mimic benign inflammatory dermatoses, and advanced disease frequently develops resistance to standard therapies, including histone deacetylase (HDAC) inhibitors. Here, we summarize how aberrant DNA methylation and histone modifications contribute to CTCL pathogenesis, promote a permissive tumor microenvironment, and enable immune escape, as well as emerging epigenetic biomarkers, such as microRNA signatures and promoter hypermethylation, that may improve diagnostic accuracy and patient stratification. Finally, we discuss resistance mechanisms linked to epigenetic plasticity and intratumoral heterogeneity and highlight future strategies combining rational drug regimens with longitudinal single-cell profiling to improve the durability of response.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fcell.2026.1816800</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fcell.2026.1816800</link>
        <title><![CDATA[SLC40A1 (iron transporter): mechanistic regulation, role in disease pathogenesis, and prospects for targeted therapy]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Limian Huang</author><author>Lin Pan</author><author>Weiling Qin</author><author>Yihui Zhao</author><author>Yanyun Huang</author><author>Xiao Qin</author>
        <description><![CDATA[Solute carrier family 40 member 1 (SLC40A1) encodes ferroportin 1 (FPN1), the only known iron efflux transporter in mammalian cells, which is critical for maintaining systemic iron homeostasis and cellular iron balance. SLC40A1 plays a key role in regulating iron homeostasis and is involved in the pathogenesis of inflammatory, fibrotic, neurodegenerative diseases, and cancer, with dysfunction linked to mutations or epigenetic silencing. Its biological functions and regulatory mechanisms are complex and diverse. This article provides an overview of SLC40A1’s molecular and biological properties, elucidates its involvement in disease progression, and evaluates its clinical potential. The study seeks to enhance understanding of SLC40A1’s mechanisms, laying the groundwork for the development of targeted therapies.]]></description>
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