Epithelial-Mesenchymal Transition in Renal Fibrosis
Summary
Renal fibrosis is a final common pathway in chronic kidney disease, characterised by excessive deposition of extracellular matrix and loss of normal architecture. Central to this process is epithelial-mesenchymal transition (EMT), during which injured renal tubular epithelial cells undergo phenotypic conversion to mesenchymal, myofibroblast-like cells. This transition involves loss of epithelial markers, such as E-cadherin, and gain of mesenchymal features, including α-smooth muscle actin (α-SMA) expression and enhanced motility. EMT is driven by profibrotic cytokines—most notably transforming growth factor-β1 (TGF-β1)—and by epigenetic and metabolic modulators. Persistent EMT contributes to interstitial myofibroblast accumulation and progressive scarring, ultimately impairing glomerular filtration and tubular function. Understanding the molecular regulators of EMT has therefore become fundamental to developing anti-fibrotic therapies that might preserve renal function in diverse forms of kidney injury.
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Epithelial-Mesenchymal Transition in Renal Fibrosis publication trend
The graph below shows the total number of articles in epithelial-mesenchymal transition in renal fibrosis across all publications each year (not limited to Nature Index journals).
Technical terms
Epithelial-Mesenchymal Transition (EMT): A biological programme whereby epithelial cells lose polarity and adhesion to acquire migratory, mesenchymal characteristics, contributing to fibrosis.
Transforming Growth Factor-β1 (TGF-β1): A cytokine that orchestrates pro-fibrotic signalling cascades, inducing EMT and extracellular matrix accumulation.
Myofibroblast: A contractile, fibroblast-like cell expressing α-SMA, responsible for excessive matrix deposition in fibrotic tissue.
E-cadherin: An epithelial adherens junction protein whose downregulation marks the initiation of EMT.
α-Smooth Muscle Actin (α-SMA): A cytoskeletal protein upregulated during EMT, indicative of mesenchymal and myofibroblast differentiation.
References
- METTL14-regulated PI3K/Akt signaling pathway via PTEN affects HDAC5-mediated epithelial–mesenchymal transition of renal tubular cells in diabetic kidney disease. Cell Death & Disease (2021).
- PP2 Ameliorates Renal Fibrosis by Regulating the NF‐κB/COX‐2 and PPARγ/UCP2 Pathway in Diabetic Mice. Oxidative Medicine and Cellular Longevity (2021).
- Magnoflorine Ameliorates Inflammation and Fibrosis in Rats With Diabetic Nephropathy by Mediating the Stability of Lysine-Specific Demethylase 3A. Frontiers in Physiology (2020).
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