ArticleAmerican journal of physiology. Renal physiology2011
Genetic deficiency of Smad3 protects against murine ischemic acute kidney injury.
Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- 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
- Early single session of hyperbaric oxygen therapy mitigates renal apoptosis in lipopolysaccharides-induced endotoxemia in rats.Kidney research and clinical practice · 2025Article
- Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals.Inflammopharmacology · 2022Review
- Smad3 promotes adverse cardiovascular remodeling and dysfunction in doxorubicin-treated hearts.American journal of physiology. Heart and circulatory physiology · 2022Article
- BMPER alleviates ischemic brain injury by protecting neurons and inhibiting neuroinflammation via Smad3-Akt-Nrf2 pathway.CNS neuroscience & therapeutics · 2022Article
- SIS3 Alleviates Cisplatin-Induced Acute Kidney Injury by Regulating the LncRNA Arid2-IR-Transferrin Receptor Pathway.Kidney & blood pressure research · 2022Article
- Smad3 Signatures in Renal Inflammation and Fibrosis.International journal of biological sciences · 2022Review
- Smad3-Targeted Therapy Protects against Cisplatin-Induced AKI by Attenuating Programmed Cell Death and Inflammation via a NOX4-Dependent Mechanism.Kidney diseases (Basel, Switzerland) · 2021Article
- TGF-Beta as a Master Regulator of Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- Proximal tubule LPA1 and LPA2 receptors use divergent signaling pathways to additively increase profibrotic cytokine secretion.American journal of physiology. Renal physiology · 2021Article
- Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury.International journal of biological sciences · 2021Review
- Smad3 promotes AKI sensitivity in diabetic mice via interaction with p53 and induction of NOX4-dependent ROS production.Redox biology · 2020Article
- Heme oxygenase-2 protects against ischemic acute kidney injury: influence of age and sex.American journal of physiology. Renal physiology · 2019Article
- The many talents of transforming growth factor-β in the kidney.Current opinion in nephrology and hypertension · 2019Review
- Conditional knockout of TGF-βRII /Smad2 signals protects against acute renal injury by alleviating cell necroptosis, apoptosis and inflammation.Theranostics · 2019Article
- The Impact of Versatile Macrophage Functions on Acute Kidney Injury and Its Outcomes.Frontiers in physiology · 2019Article
- Ccl2 deficiency protects against chronic renal injury in murine renovascular hypertension.Scientific reports · 2018Article
- AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms.Kidney international · 2017Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
TGF-β1 contributes to chronic kidney disease, at least in part, via Smad3. TGF-β1 is induced in the kidney following acute ischemia, and there is increasing evidence that TGF-β1 may protect against acute kidney injury. As there is a paucity of information regarding the functional significance of Smad3 in acute kidney injury, the present study explored this issue in a murine model of ischemic acute kidney injury in Smad3(+/+) and Smad3(-/-) mice. We demonstrate that, at 24 h after ischemia, Smad3 is significantly induced in Smad3(+/+) mice, whereas Smad3(-/-) mice fail to express this protein in the kidney in either the sham or postischemic groups. Compared with Smad3(+/+) mice, and 24 h following ischemia, Smad3(-/-) mice exhibited greater preservation of renal function as measured by blood urea nitrogen (BUN) and serum creatinine; less histological injury assessed by both semiquantitative and qualitative analyses; markedly suppressed renal expression of IL-6 and endothelin-1 mRNA (but comparable expression of MCP-1, TNF-α, and heme oxygenase-1 mRNA); and no increase in plasma IL-6 levels, the latter increasing approximately sixfold in postischemic Smad3(+/+) mice. We conclude that genetic deficiency of Smad3 confers structural and functional protection against acute ischemic injury to the kidney. We speculate that these effects may be mediated through suppression of IL-6 production. Finally, we suggest that upregulation of Smad3 after an ischemic insult may contribute to the increased risk for chronic kidney disease that occurs after acute renal ischemia.
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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.