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Abstract INTRODUCTION RESULTS DISCUSSION MATERIALS AND METHODS Acknowledgments Supplementary Materials REFERENCES Information & Authors Metrics & Citations View Options References Figures Tables Media Share This article has 0 eLetter . Abstract Fibrosis, marked by excess extracellular matrix (ECM) deposition, is the end stage of many diseases. Single-cell studies have highlighted the emergence of disease-specific fibroblast populations, including a high collagen–synthesizing CTHRC1+ subpopulation.
Abstract Fibrosis is a chronic disease characterized by excessive extracellular matrix production, which leads to disruption of organ function. Fibroblasts are key effector cells of this process, responding chiefly to the pleiotropic cytokine transforming growth factor–β1 (TGF-β1), which promotes fibroblast to myofibroblast differentiation.
Abstract Fibrosis is a chronic disease characterized by excessive extracellular matrix (ECM) production which leads to destruction of normal tissue architecture and disruption of organ function. Fibroblasts are key effector cells of this process and respond to a host of pro-fibrotic stimuli, including notably the pleiotropic cytokine, TGF-β1, which promotes fibroblast to myofibroblast differentiation.
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