About this Research Topic
Fibrosis, a characteristic of all chronic kidney diseases (CKD), is now recognized to be an independent predictor of disease progression. Renal fibrosis is a complex process characterized by excessive extracellular matrix (ECM) accumulation, leading to structural damage and progressive loss of renal function. Despite this critical impact, no targeted therapy yet exists to slow renal fibrosis. Understanding the molecular mechanisms underlying kidney fibrosis is crucial for developing effective therapies.
The process of renal fibrosis involves a complex interplay of various cellular and molecular mechanisms, which are still being actively investigated. The immune response plays a key role, including interactions between immune cells and other cell types, as well as inflammation, which can promote fibroblast activation. Recent advances in epigenetics, transcriptomics, genetics, and cell-specific gene ablation techniques have enabled functional studies of genes, identifying novel mechanisms and molecular markers for fibrosis pathogenesis, thus providing insights into potential therapeutic targets.
Autophagy, a cellular process responsible for degrading damaged cellular components, is also implicated in renal fibrosis. Dysregulation of autophagy can contribute to the accumulation of pro-fibrotic factors, promoting fibrosis. Furthermore, network analyses of genome-wide transcriptome studies have identified metabolism as one of the top dysregulated pathways in the diseased kidneys. Metabolic reprogramming, including mitochondrial dysfunction, glycolysis, and fatty acid oxidation, has been shown to play a key role in renal fibrosis.
Further research is needed to elucidate the intricate mechanisms underlying renal fibrosis and to develop novel therapeutic strategies targeting specific molecular pathways. Therefore, this research topic aims to gather a collection of articles covering recent advances of renal fibrosis pathogenesis, ultimately contributing to improved therapeutic interventions and non-invasive diagnostic tools. Submission of Original Research, Review and Mini-Review, and Clinical Trial are particularly welcome.
This research aims to uncover novel and valuable knowledge about the functions and regulatory mechanisms of renal fibrosis, particularly in the context of renal transplantation. The goal is to identify promising therapeutic targets and strategies that can improve CKD and enhance renal allograft survival.
This Research Topic accepts Original Research, Review and Mini-Review, Clinical Trial. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
• Cell crosstalk and interaction in tissue microenvironment of renal fibrosis
• Function of immune cells in renal allograft fibrosis
• Epigenetic regulation in renal fibrosis
• Genetics and transcriptomics of renal fibrosis
• Inflammation and autophagy in renal fibrosis
• The role of cell metabolism in renal fibrosis
• Novel molecular targets or pharmaceuticals for renal fibrosis
• Novel biomarkers for diagnosis and prognosis of renal fibrosis
• Clinical trials in renal fibrosis and renal allograft survival.
The process of renal fibrosis involves a complex interplay of various cellular and molecular mechanisms, which are still being actively investigated. The immune response plays a key role, including interactions between immune cells and other cell types, as well as inflammation, which can promote fibroblast activation. Recent advances in epigenetics, transcriptomics, genetics, and cell-specific gene ablation techniques have enabled functional studies of genes, identifying novel mechanisms and molecular markers for fibrosis pathogenesis, thus providing insights into potential therapeutic targets.
Autophagy, a cellular process responsible for degrading damaged cellular components, is also implicated in renal fibrosis. Dysregulation of autophagy can contribute to the accumulation of pro-fibrotic factors, promoting fibrosis. Furthermore, network analyses of genome-wide transcriptome studies have identified metabolism as one of the top dysregulated pathways in the diseased kidneys. Metabolic reprogramming, including mitochondrial dysfunction, glycolysis, and fatty acid oxidation, has been shown to play a key role in renal fibrosis.
Further research is needed to elucidate the intricate mechanisms underlying renal fibrosis and to develop novel therapeutic strategies targeting specific molecular pathways. Therefore, this research topic aims to gather a collection of articles covering recent advances of renal fibrosis pathogenesis, ultimately contributing to improved therapeutic interventions and non-invasive diagnostic tools. Submission of Original Research, Review and Mini-Review, and Clinical Trial are particularly welcome.
This research aims to uncover novel and valuable knowledge about the functions and regulatory mechanisms of renal fibrosis, particularly in the context of renal transplantation. The goal is to identify promising therapeutic targets and strategies that can improve CKD and enhance renal allograft survival.
This Research Topic accepts Original Research, Review and Mini-Review, Clinical Trial. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
• Cell crosstalk and interaction in tissue microenvironment of renal fibrosis
• Function of immune cells in renal allograft fibrosis
• Epigenetic regulation in renal fibrosis
• Genetics and transcriptomics of renal fibrosis
• Inflammation and autophagy in renal fibrosis
• The role of cell metabolism in renal fibrosis
• Novel molecular targets or pharmaceuticals for renal fibrosis
• Novel biomarkers for diagnosis and prognosis of renal fibrosis
• Clinical trials in renal fibrosis and renal allograft survival.
Keywords: Renal fibrosis, renal transplantation, microenvironment, epigenetics, transcriptomics, cell metabolism, autophagy, biomarkers, clinical trials
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
