About this Research Topic
Tissue fibrosis leads to organ failure and significant morbidity worldwide, with over 30% of disabling and fatal diseases attributed to the deleterious effects of organ fibrosis. Among these, pulmonary fibrosis stands as a menacing lung disorder characterized by the replacement of healthy lung architecture with maladaptive tissue remodeling and deposition of extracellular matrix (ECM), leading to profound architectural distortions, aberrant signaling, and ultimately, organ dysfunction. Fibroblasts and myofibroblasts participate in tissue homeostasis and are considered the primary cell types that orchestrate the maladaptive tissue remodeling and excessive extracellular matrix accumulation. Recently, rapid advancements in genetic and transcriptomic technologies have propelled our understanding of cell heterogeneity and intricate molecular and cellular changes in a spatiotemporal manner in the fibrotic lungs.
This Research Topic will highlight advances in the understanding of the complexity and heterogeneity of cell types, and their molecular and cellular mechanisms contributing to extracellular matrix deposition and fibrotic tissue remodeling. Recent evidence suggests a more complex pattern of cell phenotypes in idiopathic pulmonary fibrosis (IPF) lungs, including increased epithelial cell heterogeneity, the emergence of fibroblast and myofibroblast subtypes, the discovery of aberrant endothelial cells and profibrotic macrophages, as well as crosstalk between different cell types that elicit profibrotic effects. In a spatiotemporal manner, these key cells and their subtypes further confound the pathogenesis of lung fibrosis and other tissue fibrosis. A better understanding of these cell types will elucidate the mechanisms involved in tissue remodeling during fibrosis development and progression. Authors are highly encouraged to submit a wide range of articles, including cellular signaling-based studies, omics-based studies pertaining to tissue fibrosis, mechanistic understandings based on animal models, as well as articles elucidating advanced mechanisms for understanding tissue remodeling and fibrosis.
We invite submissions of diverse article types (including Original Research, Brief Research Reports, Reviews, and Mini-Reviews) that address, but are not limited to, the following areas of interest:
• New insights into cell heterogeneity in the pathogenesis of tissue remodeling and fibrosis
• New Insights into cellular and molecular mechanisms of tissue remodeling and fibrosis
• Mechanisms by which cell-cell crosstalk promotes or demotes profibrotic reactions and ECM remodeling
• Methodology and models for studying a certain cell type for tissue remodeling and fibrosis
• The roles of different cell types in fibrosis
• Therapeutic strategies for the prevention and treatment of lung injury and fibrosis.
More information on article types accepted by the journal can be found here.
Please note: descriptive studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
This Research Topic will highlight advances in the understanding of the complexity and heterogeneity of cell types, and their molecular and cellular mechanisms contributing to extracellular matrix deposition and fibrotic tissue remodeling. Recent evidence suggests a more complex pattern of cell phenotypes in idiopathic pulmonary fibrosis (IPF) lungs, including increased epithelial cell heterogeneity, the emergence of fibroblast and myofibroblast subtypes, the discovery of aberrant endothelial cells and profibrotic macrophages, as well as crosstalk between different cell types that elicit profibrotic effects. In a spatiotemporal manner, these key cells and their subtypes further confound the pathogenesis of lung fibrosis and other tissue fibrosis. A better understanding of these cell types will elucidate the mechanisms involved in tissue remodeling during fibrosis development and progression. Authors are highly encouraged to submit a wide range of articles, including cellular signaling-based studies, omics-based studies pertaining to tissue fibrosis, mechanistic understandings based on animal models, as well as articles elucidating advanced mechanisms for understanding tissue remodeling and fibrosis.
We invite submissions of diverse article types (including Original Research, Brief Research Reports, Reviews, and Mini-Reviews) that address, but are not limited to, the following areas of interest:
• New insights into cell heterogeneity in the pathogenesis of tissue remodeling and fibrosis
• New Insights into cellular and molecular mechanisms of tissue remodeling and fibrosis
• Mechanisms by which cell-cell crosstalk promotes or demotes profibrotic reactions and ECM remodeling
• Methodology and models for studying a certain cell type for tissue remodeling and fibrosis
• The roles of different cell types in fibrosis
• Therapeutic strategies for the prevention and treatment of lung injury and fibrosis.
More information on article types accepted by the journal can be found here.
Please note: descriptive studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
Keywords: tissue remodeling, extracellular matrix, Tissue Fibrosis, Pulmonary Fibrosis, Molecular and Cellular Mechanisms, Profibrotic Effect, Fibroblast and Myofibroblast, Cell Heterogeneity
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.
