ArticleJournal of molecular medicine (Berlin, Germany)2017
Angiotensin II induces calcium/calcineurin signaling and podocyte injury by downregulating microRNA-30 family members.
Article in Journal of molecular medicine (Berlin, Germany), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Emerging roles of non-coding RNAs in idiopathic nephrotic syndrome: a narrative review.BMC nephrology · 2025Review
- G-Protein-Coupled Receptors in Chronic Kidney Disease Induced by Hypertension and Diabetes.Cells · 2025Review
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- Urinary-derived extracellular vesicles reveal a distinct microRNA signature associated with the development and progression of Fabry nephropathy.Frontiers in medicine · 2023Article
- Calcineurin in development and disease.Genes & diseases · 2022Review
- Upregulated LRRC55 promotes BK channel activation and aggravates cell injury in podocytes.The Journal of experimental medicine · 2021Article
- MiR-30a-5p ameliorates LPS-induced inflammatory injury in human A549 cells and mice via targeting RUNX2.Innate immunity · 2021Article
- miR-30a-5p targets Becn1 to ameliorate high-glucose-induced glomerular podocyte injury in immortalized rat podocyte cell line.American journal of translational research · 2021Article
- MicroRNA-30/Cx43 axis contributes to podocyte injury by regulating ER stress in diabetic nephropathy.Annals of translational medicine · 2020Article
- ACE-Triggered Hypertension Incites Stroke: Genetic, Molecular, and Therapeutic Aspects.Neuromolecular medicine · 2020Review
- Immunomodulatory and Regenerative Effects of Mesenchymal Stem Cell-Derived Extracellular Vesicles in Renal Diseases.International journal of molecular sciences · 2020Review
- Association between Renal Podocalyxin Expression and Renal Dysfunction in Patients with Diabetic Nephropathy: A Single-Center, Retrospective Case-Control Study.BioMed research international · 2020Article
- Critical roles of PI3K/Akt/NF‑κB survival axis in angiotensin II‑induced podocyte injury.Molecular medicine reports · 2019Article
- The microRNA in ventricular remodeling: the miR-30 family.Bioscience reports · 2019Review
- The distinct role of CD73 in the progression of pancreatic cancer.Journal of molecular medicine (Berlin, Germany) · 2019Article
- MiR-30 family prevents uPAR-ITGB3 signaling activation through calcineurin-NFATC pathway to protect podocytes.Cell death & disease · 2019Article
- MiR-30e-5p and MiR-15a-5p Expressions in Plasma and Urine of Type 1 Diabetic Patients With Diabetic Kidney Disease.Frontiers in genetics · 2019Article
- Causes and Consequences of the Dysregulated Maternal Renin-Angiotensin System in Preeclampsia.Frontiers in endocrinology · 2019Review
- Triptolide protects podocytes from TGF-β-induced injury by preventing miR-30 downregulation.American journal of translational research · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin II (AngII) is capable of inducing calcium/calcineurin signaling and podocyte injury; however, the precise underlying mechanism is not well understood. Because we have previously demonstrated that microRNA-30s (miR-30s) inhibit calcium/calcineurin signaling in podocytes, we hypothesize that AngII may induce podocyte injury by downregulating miR-30s and thereby activating calcium/calcineurin signaling. To test this hypothesis, we used an AngII-induced podocyte injury mouse model. The mice were treated with AngII via infusion for 28 days, which resulted in hypertension, albuminuria, and glomerular damage. AngII treatment also resulted in a significant reduction of miR-30s and upregulation of calcium/calcineurin signaling components, including TRPC6, PPP3CA, PPP3CB, PPP3R1, and NFATC3, which are the known targets of miR-30s in podocytes. The delivery of miR-30a-expressing lentivirus to the podocytes on day 14 of the infusion ameliorated the AngII-induced podocyte and glomerular injury and attenuated the upregulation of the calcium/calcineurin signaling components. Similarly, treatment with losartan, which is an AngII receptor blocker, also prevented AngII-induced podocyte injury and calcium/calcineurin signaling activation. Notably, losartan was found to sustain miR-30 levels during AngII treatment both in vivo and in vitro. In conclusion, the effect of AngII on podocytes is in part mediated by miR-30s through calcium/calcineurin signaling, a novel mechanism underlying AngII-induced podocyte injury. KEY MESSAGES: • AngII infusion resulted in downregulation of miR-30s in podocytes. • Exogenous miR-30a delivery mitigated the glomerular and podocyte injuries induced by AngII. • Both miR-30a and losartan prevented AngII-induced activation of calcium-calcineurin signaling.
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