ReviewCurrent opinion in nephrology and hypertension2019
The many talents of transforming growth factor-β in the kidney.
Review in Current opinion in nephrology and hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Novel biomarkers for CKD risk stratification: a literature review.Jornal brasileiro de nefrologia · 2026Review
- Cardiac LIM Protein, Kidney Fibrosis, and Vascular Change after Acute Cardiorenal Syndrome.Journal of the American Society of Nephrology : JASN · 2025Article
- Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).International journal of molecular medicine · 2025Review
- LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Epithelial cell states associated with kidney and allograft injury.Nature reviews. Nephrology · 2024Review
- Transcriptomic, epigenomic, and spatial metabolomic cell profiling redefines regional human kidney anatomy.Cell metabolism · 2024Article
- Fibrosis in Chronic Kidney Disease: Pathophysiology and Therapeutic Targets.Journal of clinical medicine · 2024Review
- Article
- GPR97 deficiency ameliorates renal interstitial fibrosis in mouse hypertensive nephropathy.Acta pharmacologica Sinica · 2023Article
- Inhibition of Transforming Growth Factor-β Improves Primary Renal Tubule Cell Differentiation in Long-Term Culture.Tissue engineering. Part A · 2023Article
- Therapeutic Ultrasound Halts Progression of Chronic Kidney Disease In Vivo via the Regulation of Markers Associated with Renal Epithelial-Mesenchymal Transition and Senescence.International journal of molecular sciences · 2022Article
- Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies.International journal of molecular sciences · 2022Review
- IL-15 Prevents Renal Fibrosis by Inhibiting Collagen Synthesis: A New Pathway in Chronic Kidney Disease?International journal of molecular sciences · 2021Article
- Transforming growth factor beta signaling functions during mammalian kidney development.Pediatric nephrology (Berlin, Germany) · 2021Review
- miR299a-5p promotes renal fibrosis by suppressing the antifibrotic actions of follistatin.Scientific reports · 2021Article
- Podocyte and endothelial-specific elimination of BAMBI identifies differential transforming growth factor-β pathways contributing to diabetic glomerulopathy.Kidney international · 2020Article
- Biomarkers of Chronic Renal Tubulointerstitial Injury.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewPreclinical data suggests that transforming growth factor-β (TGF-β) is arguably the most potent profibrotic growth factor in kidney injury. Despite this, recent clinical trials targeting TGF-β have been disappointing. These negative studies suggest that TGF-β signaling in the injured kidney might be more complicated than originally thought. This review examines recent studies that expand our understanding of how this pleiotropic growth factor affects renal injury. RECENT
findingsThere are recent studies showing new mechanisms whereby TGF-β can mediate injury (e.g. epigenetic effects, macrophage chemoattractant). However, more significant are the increasing reports on cross-talk between TGF-β signaling and other pathways relevant to renal injury such as Wnt/β-catenin, YAP/TAZ (transcriptional coactivator with PDZ-binding motif), and klotho/FGF23. TGF-β clearly alters the response to injury, not just by direct transcriptional changes on target cells, but also through effects on other signaling pathways. In T cells and tubular epithelial cells, some of these TGF-β-mediated changes are potentially beneficial. SUMMARY: It is unlikely that inhibition of TGF-β per se will be a successful antifibrotic strategy, but a better understanding of TGF-β's actions may reveal promising downstream targets or modulators of signaling to target therapeutically for chronic kidney disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.