Transforming Growth Factor Beta Signaling in Renal Pathologies
Summary
Transforming Growth Factor Beta (TGF-β) occupies a central position in the regulation of renal homeostasis and the pathogenesis of chronic kidney disease. In physiological settings, tightly controlled TGF-β activity ensures balanced cell proliferation, differentiation and repair. In contrast, sustained activation of TGF-β drives a cascade of events leading to epithelial-to-mesenchymal transition, fibroblast activation and excessive deposition of extracellular matrix. Canonical signalling proceeds via ligand binding to type I and II receptors, phosphorylation of receptor-regulated Smad2 and Smad3, and nuclear translocation of Smad complexes to regulate target genes. This axis is counterbalanced by inhibitory Smad7 and by non-canonical pathways involving MAP kinases, Rho GTPases and PI3K/Akt. Emerging evidence highlights the importance of non-coding RNAs, epigenetic modifiers and post-translational regulators in shaping the TGF-β response. Dysregulation of these modulators underlies fibrotic scarring in diverse renal insults, including diabetic nephropathy, hypertensive injury and ureteric obstruction, and positions the TGF-β network as both a biomarker reservoir and a therapeutic target in preventing progression to end-stage renal disease.
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Transforming Growth Factor Beta Signaling in Renal Pathologies publication trend
The graph below shows the total number of articles in transforming growth factor beta signaling in renal pathologies across all publications each year (not limited to Nature Index journals).
Technical terms
Transforming Growth Factor Beta (TGF-β): A pleiotropic cytokine that controls cell growth, differentiation and extracellular matrix production.
Smad proteins: Intracellular transcription factors that convey signals from activated TGF-β receptors to the nucleus.
Renal fibrosis: Excessive accumulation of extracellular matrix in the kidney, leading to organ dysfunction.
Deacetylation: Enzymatic removal of acetyl groups from lysine residues, influencing protein stability and activity.
Epigenetic regulation: Heritable chromatin modifications, such as histone methylation, that modulate gene transcription.
Ubiquitination: Attachment of ubiquitin to target proteins, commonly marking them for proteasomal degradation.
References
- SIRT2 alleviated renal fibrosis by deacetylating SMAD2 and SMAD3 in renal tubular epithelial cells. Cell Death & Disease (2023).
- SETD2 deficiency promotes renal fibrosis through the TGF‐β/Smad signalling pathway in the absence of VHL. Clinical and Translational Medicine (2023).
- TGF-β/Smad signaling in renal fibrosis. Frontiers in Physiology (2015).
- Diverse Role of TGF-β in Kidney Disease. Frontiers in Cell and Developmental Biology (2020).
- Transforming Growth Factor-Beta1 in Diabetic Kidney Disease. Frontiers in Cell and Developmental Biology (2020).
About these summaries
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