ArticleMedical science monitor : international medical journal of experimental and clinical research2016
TRPC6 May Protect Renal Ischemia-Reperfusion Injury Through Inhibiting Necroptosis of Renal Tubular Epithelial Cells.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Polysaccharide Peptide fromBiomolecules · 2026Article
- The roles of TRPC6 in renal tubular disorders: a narrative review.Renal failure · 2024Review
- TRPC6 Knockout Alleviates Renal Fibrosis through PI3K/AKT/GSK3B Pathway.Current medical science · 2024Article
- Renal ischaemia-reperfusion injury is promoted by transcription factor NF-kB p65, which inhibits TRPC6 expression by activating miR-150.Clinical hemorheology and microcirculation · 2024Article
- A Putative Role for TRPC6 in Immune-Mediated Kidney Injury.International journal of molecular sciences · 2023Review
- TRPC Channels in the Physiology and Pathophysiology of the Renal Tubular System: What Do We Know?International journal of molecular sciences · 2022Review
- TRPC6 ameliorates renal ischemic reperfusion injury by inducing ZnAnnals of translational medicine · 2022Article
- Protective effects of dapagliflozin against oxidative stress-induced cell injury in human proximal tubular cells.PloS one · 2021Article
- MiR-124 Negatively Regulated PARP1 to Alleviate Renal Ischemia-reperfusion Injury by Inhibiting TNFα/RIP1/RIP3 Pathway.International journal of biological sciences · 2021Article
- Mesenchymal Stem/Stromal Cells and their Extracellular Vesicle Progeny Decrease Injury in Poststenotic Swine Kidney Through Different Mechanisms.Stem cells and development · 2020Article
- Necrostatin-1 Attenuates Renal Ischemia and Reperfusion Injury via Meditation of HIF-1α/mir-26a/TRPC6/PARP1 Signaling.Molecular therapy. Nucleic acids · 2019Article
- Review
- Detection of Necroptosis in Ligand-Mediated and Hypoxia-Induced Injury of Hepatocytes Using a Novel Optic Probe-Detecting Receptor-Interacting Protein (RIP)1/RIP3 Binding.Oncology research · 2018Article
- Protective Effect of Luteolin Against Renal Ischemia/Reperfusion Injury via Modulation of Pro-Inflammatory Cytokines, Oxidative Stress and Apoptosis for Possible Benefit in Kidney Transplant.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to explore the potential role of TRPC6 in the pathophysiology of HK-2 cell injury following ischemia reperfusion (I/R). MATERIAL AND METHODS TRPC6 expression was analyzed by immunofluorescence staining. siRNA was transfected to knockout of TRPC6 in HK-2 cells, and in vitro I/R was then induced. Cell apoptosis and necrosis were determined by Annexin V-FITC/PI staining. Necroptosis was determined by necrostatin-1 and expressions of necroptosis-related proteins were evaluated. OAG, SKF96365, or KN-93 was further used to interfere with TRPC6 expression. RESULTS Cytoplasmic TRPC6 expression was demonstrated. I/R induced TRPC6 expression in normal or NC siRNA-transfected cells but not in TRPC6 siRNA-knockout ones. There was a progressive increase in apoptotic and necrotic cells with increasing reoxygenation time in all 3 groups, while necrosis in TRPC6 siRNA-transfected cells was comparatively higher than that of the other 2 groups (p<0.05). Expressions of necroptosis-related proteins were interfered with following I/R and these effects were enhanced by TRPC6 siRNA. Application of OAG, SKF96365, or KN93 further affected necroptosis following I/R. CONCLUSIONS This study described the expression and functional relevance of TRPC6 in the pathophysiology of HK-2 cell following I/R. Our results regarding the ability of TRPC6 to specifically interrupt necroptosis may shed new light on its role in prevention and control of ischemic kidney injury.
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