ArticleKidney international2016
Hypoxia-inducible factor-1α promotes glomerulosclerosis and regulates COL1A2 expression through interactions with Smad3.
Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 85 citations in OpenAlex.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Glycohypoxia: a hypothesis linking chronic hyperglycemia to functional hypoxia and diabetic complications in type 2 diabetes.Medical gas research · 2026Review
- Dangguibuxue Decoction Attenuated AA I-Induced Renal Fibrosis: Integrating Network Pharmacology and Experimental Validation.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Direct pharmacological targeting of Piezo1 by Paeoniflorin: a novel therapeutic approach for renal fibrosis.Journal of advanced research · 2026Article
- Adipokine networks in diabetic kidney disease: mechanistic insights and therapeutic implications.Lipids in health and disease · 2026Review
- Hypoxia-inducible factor-1α promotes tubulointerstitial fibrosis via the upregulation ofRenal failure · 2025Article
- When in doubt, pig it out: a versatile translational platform to study CKD, HFpEF, and CKM syndrome.American journal of physiology. Heart and circulatory physiology · 2025Review
- Exosomal miR-122-5p from tubular cells ameliorates renal interstitial fibrosis by regulating fibroblasts via HIF-1α.Cell death discovery · 2025Article
- Hypoxia amplifies arecoline-induced invasion and metastasis in oral squamous cell carcinoma - Insights into TGF-β1 signaling and collagen production.Journal of dental sciences · 2025Article
- Identifying potential drugs for treating Cardiovascular-kidney metabolic syndrome via reverse network pharmacology.Frontiers in pharmacology · 2025Article
- Roxadustat regulates the cell cycle and inhibits proliferation of mesangial cells via the hypoxia-inducible factor-1α/P53/P21 pathway.Frontiers in cell and developmental biology · 2025Article
- Mesenchymal Stem Cell-conditioned Medium Attenuated CoClCurrent pharmaceutical design · 2025Article
- HIF-1 contributes to autophagy activation via BNIP3 to facilitate renal fibrosis in hypoxia in vitro and UUO in vivo.American journal of physiology. Cell physiology · 2024Article
- Challenges and opportunities in obesity: the role of adipocytes during tissue fibrosis.Frontiers in endocrinology · 2024Review
- Glomerular injury after trauma, burn, and sepsis.Journal of nephrology · 2023Review
- Hypoxia-induced signaling in the cardiovascular system: pathogenesis and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- The impact of hypoxia-inducible factors in the pathogenesis of kidney diseases: a link through cell metabolism.Kidney research and clinical practice · 2023Article
- Activation of HIF-1α C-terminal transactivation domain protects against hypoxia-induced kidney injury through hexokinase 2-mediated mitophagy.Cell death & disease · 2023Article
- VHL-recruiting PROTAC attenuates renal fibrosis and preserves renal function via simultaneous degradation of Smad3 and stabilization of HIF-2α.Cell & bioscience · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The function of hypoxia-inducible factor-1α (HIF-1α) in chronic kidney disease is disputed. Here we report that interactions of HIF-1α with transforming growth factor-β (TGF-β) signaling may promote its fibrotic effects. Knockout of HIF-1α is protective against glomerulosclerosis and glomerular type-I collagen accumulation in a mouse podocyte ablation model. Transcriptional analysis of cultured renal cells showed that α2(I) collagen expression is directly regulated by HIF-1α binding to a functional hypoxia-responsive element in its promoter at -335 relative to the transcription start site. Activation of COL1A2 transcription by HIF-1α occurred in the absence of hypoxia and is strongly enhanced by TGF-β signaling. TGF-β, in addition to increasing HIF-1α levels, increased both HIF-1α binding to the COL1A2 promoter and HIF-1α N-terminal transactivation domain activity. These effects of TGF-β on HIF-1α were inhibited in Smad3-null mouse embryonic fibroblasts, suggesting a requirement for Smad3. Phosphorylated Smad3 also associated with the -335 hypoxia-responsive element of the COL1A2 promoter independent of a Smad DNA binding sequence. Smad3 binding to the -335 hypoxia-responsive element required HIF-1α both in vitro and in kidney lysate from the disease model, suggesting formation of an HIF-1α-Smad3 transcriptional complex. Thus, HIF-1α-Smad3 has a novel interaction in glomerulosclerosis.
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