ArticleFrontiers in medicine2021
TRPC5 Channel Inhibition Protects Podocytes in Puromycin-Aminonucleoside Induced Nephrosis Models.
Article in Frontiers in medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Taming renal inflammation: signaling pathways and therapeutic advances in lupus nephritis.BMC nephrology · 2025Review
- Revisiting nephrin signaling and its specialized effects on the uniquely adaptable podocyte.The Biochemical journal · 2025Review
- Effects of Graphene Quantum Dots on Renal Fibrosis Through Alleviating Oxidative Stress and Restoring Mitochondrial Membrane Potential.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The small GTPase regulatory protein Rac1 drives podocyte injury independent of cationic channel protein TRPC5.Kidney international · 2023Article
- Role of ion channels in the mechanism of proteinuria (Review).Experimental and therapeutic medicine · 2023Review
- Ion channels and channelopathies in glomeruli.Physiological reviews · 2023Review
- The Role of Connexin 43 in Renal Disease: Insights from In Vivo Models of Experimental Nephropathy.International journal of molecular sciences · 2022Review
- Transplanted organoids empower human preclinical assessment of drug candidate for the clinic.Science advances · 2022Article
- TRPC6 Inactivation Reduces Albuminuria Induced by Protein Overload in Sprague Dawley Rats.Cells · 2022Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Podocyte injury and the appearance of proteinuria are key features of several progressive kidney diseases. Genetic deletion or selective inhibition of TRPC5 channels with small-molecule inhibitors protects podocytes in rodent models of kidney disease, but less is known about the human relevance and translatability of TRPC5 inhibition. Here, we investigate the effect of TRPC5 inhibition in puromycin aminonucleoside (PAN)-treated rats, human iPSC-derived podocytes, and kidney organoids. We first established that systemic administration of the TRPC5 inhibitor AC1903 was sufficient to protect podocyte cytoskeletal proteins and suppress proteinuria in PAN-induced nephrosis rats, an established model of podocyte injury. TRPC5 current was recorded in the human iPSC-derived podocytes and was blocked by AC1903. PAN treatment caused podocyte injury in human iPSC-derived podocytes and kidney organoids. Inhibition of TRPC5 channels reversed the effects of PAN-induced injury in human podocytes in both 2D and 3D culture systems. Taken together, these results revealed the relevance of TRPC5 channel inhibition in puromycin-aminonucleoside induced nephrosis models, highlighting the potential of this therapeutic strategy for patients.
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