ArticleMolecular endocrinology (Baltimore, Md.)2011
Calcineurin (CN) activation promotes apoptosis of glomerular podocytes both in vitro and in vivo.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Efficacy and safety of immunosuppressive agents for adults with lupus nephritis: a systematic review and network meta-analysis.Frontiers in immunology · 2023Pooled it
- Trial
- Tacrolimus is an alternative therapy option for the treatment of adult steroid-resistant nephrotic syndrome: a prospective, multicenter clinical trial.International urology and nephrology · 2013Trial
- Eicosanoids as Biomarkers of Hyperfiltration-Mediated Injury in CKD.Kidney international reports · 2026Article
- Tacrolimus and diabetic rodent models.Pharmacological reports : PR · 2025Review
- The case for treatment of monogenic SRNS with calcineurin inhibitors.Kidney international · 2023Article
- Unraveling the Crosstalk between Lipids and NADPH Oxidases in Diabetic Kidney Disease.Pharmaceutics · 2023Review
- Multicentric Carpotarsal Osteolysis Syndrome Associated Nephropathy: Novel Variants ofJournal of clinical medicine · 2022Article
- How immunosuppressive drugs may directly target podocytes in glomerular diseases.Pediatric nephrology (Berlin, Germany) · 2022Review
- Lipopolysaccharide-induced podocyte injury is regulated by calcineurin/NFAT and TLR4/MyD88/NF-κB signaling pathways through angiopoietin-like protein 4.Genes & diseases · 2022Article
- Glomerular Biomechanical Stress and Lipid Mediators during Cellular Changes Leading to Chronic Kidney Disease.Biomedicines · 2022Review
- GAP-43 ameliorates Podocyte injury by decreasing nuclear NFATc1 expression.Biochemistry and biophysics reports · 2021Article
- Identification of Genomic Regions Influencing N-Metabolism and N-Excretion in Lactating Holstein- Friesians.Frontiers in genetics · 2021Article
- Tacrolimus Protects Podocytes from Apoptosis via Downregulation of TRPC6 in Diabetic Nephropathy.Journal of diabetes research · 2021Article
- Modulation of proteomic and inflammatory signals by Bradykinin in podocytes.Journal of advanced research · 2020Article
- TRPC Channels in Proteinuric Kidney Diseases.Cells · 2019Review
- MiR-30 family prevents uPAR-ITGB3 signaling activation through calcineurin-NFATC pathway to protect podocytes.Cell death & disease · 2019Article
- Protective Effects of Nargenicin A1 against Tacrolimus-Induced Oxidative Stress in Hirame Natural Embryo Cells.International journal of environmental research and public health · 2019Article
- Knockout of TRPC6 promotes insulin resistance and exacerbates glomerular injury in Akita mice.Kidney international · 2019Article
- Tocotrienol Rich Fraction Supplementation Modulate Brain Hippocampal Gene Expression in APPswe/PS1dE9 Alzheimer's Disease Mouse Model.Journal of Alzheimer's disease : JAD · 2019Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
To determine the role of Gq signaling and calcineurin (CN) activation in promoting apoptosis of glomerular podocytes, constitutively active Gq [Gq(+)] or CN [CN(+)] proteins were introduced into cultured podocytes using protein transduction by tagging the proteins with the transactivator of transcription peptide. To investigate the role of CN in promoting podocyte apoptosis in vivo, a genetic model of type 1 diabetes mellitus (Akita mice) was treated with the CN inhibitor FK506. In cultured podocytes, Gq(+) stimulated nuclear translocation of nuclear factor of activated T cells (NFAT) family members, activated an NFAT reporter construct, and enhanced podocyte apoptosis in a CN-dependent fashion. CN(+) similarly promoted podocyte apoptosis, and apoptosis induced by either angiotensin II or endothelin-1 was blocked by FK506. Induction of apoptosis required NFAT-induced gene transcription because apoptosis induced by either Gq(+) or CN(+) was blocked by an inhibitor that prevented CN-dependent NFAT activation without affecting CN phosphatase activity. Podocyte apoptosis was mediated, in part, by the NFAT-responsive gene cyclooxygenase 2 (COX2) and prostaglandin E(2) generation because apoptosis induced by Gq(+) was attenuated by either COX2 inhibition or blockade of the Gq-coupled E-series prostaglandins receptor. The findings appeared relevant to podocyte apoptosis in diabetic nephropathy because apoptosis was significantly reduced in Akita mice by treatment with FK506. These data suggest that Gq stimulates CN and promotes podocyte apoptosis both in vitro and in vivo. Apoptosis requires NFAT-dependent gene transcription and is mediated, in part, by CN-dependent COX2 induction, prostaglandin E(2) generation, and autocrine activation of the Gq-coupled E-series prostaglandins receptor.
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