ArticlePloS one2014
cAMP signaling prevents podocyte apoptosis via activation of protein kinase A and mitochondrial fusion.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Expression of protein kinase A catalytic subunits in healthy and diseased mouse kidneys.Pflugers Archiv : European journal of physiology · 2026Article
- Multifaceted roles of Epac signaling in renal functions.The Biochemical journal · 2025Review
- Adriamycin-induced nephropathy models: elucidating CKD pathophysiology and advancing therapeutic strategies.Experimental animals · 2025Review
- Effects of steroid-resistant nephrotic syndrome serum on AA pathway in podocytes cultured in 3D in vitro glomerular model.Scientific reports · 2025Article
- METTL10 attenuates adriamycin-induced podocyte injury by targeting cell dedifferentiation.Scientific reports · 2025Article
- Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Nicorandil protects podocytes via modulation of antioxidative capacity in acute puromycin aminonucleoside-induced nephrosis in rats.American journal of physiology. Renal physiology · 2023Article
- Anti-ANGPTL3-FLD monoclonal antibody treatment ameliorates podocyte lesions through attenuating mitochondrial damage.Cell death & disease · 2022Article
- Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022Article
- βAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2021Review
- The complicated role of mitochondria in the podocyte.American journal of physiology. Renal physiology · 2020Article
- Bucladesine Attenuates Spatial Learning and Hippocampal Mitochondrial Impairments Induced by 3, 4-Methylenedioxymethamphetamine (MDMA).Neurotoxicity research · 2020Article
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- GDC-0879, a BRAFCell chemical biology · 2018Article
- TGR5 signalling promotes mitochondrial fission and beige remodelling of white adipose tissue.Nature communications · 2018Article
- Protein Kinase A/CREB Signaling Prevents Adriamycin-Induced Podocyte Apoptosis via Upregulation of Mitochondrial Respiratory Chain Complexes.Molecular and cellular biology · 2018Article
- Adrenomedullin ameliorates podocyte injury induced by puromycin aminonucleoside in vitro and in vivo through modulation of Rho GTPases.International urology and nephrology · 2017Article
- YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCOxidative medicine and cellular longevity · 2017Article
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Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Our previous in vitro studies suggested that cyclic AMP (cAMP) signaling prevents adriamycin (ADR) and puromycin aminonucleoside (PAN)-induced apoptosis in podocytes. As cAMP is an important second messenger and plays a key role in cell proliferation, differentiation and cytoskeleton formation via protein kinase A (PKA) or exchange protein directly activated by cAMP (Epac) pathways, we sought to determine the role of PKA or Epac signaling in cAMP-mediated protection of podocytes. In the ADR nephrosis model, we found that forskolin, a selective activator of adenylate cyclase, attenuated albuminuria and improved the expression of podocyte marker WT-1. When podocytes were treated with pCPT-cAMP (a selective cAMP/PKA activator), PKA activation was increased in a time-dependent manner and prevented PAN-induced podocyte loss and caspase 3 activation, as well as a reduction in mitochondrial membrane potential. We found that PAN and ADR resulted in a decrease in Mfn1 expression and mitochondrial fission in podocytes. pCPT-cAMP restored Mfn1 expression in puromycin or ADR-treated podocytes and induced Drp1 phosphorylation, as well as mitochondrial fusion. Treating podocytes with arachidonic acid resulted in mitochondrial fission, podocyte loss and cleaved caspase 3 production. Arachidonic acid abolished the protective effects of pCPT-cAMP on PAN-treated podocytes. Mdivi, a mitochondrial division inhibitor, prevented PAN-induced cleaved caspase 3 production in podocytes. We conclude that activation of cAMP alleviated murine podocyte caused by ADR. PKA signaling resulted in mitochondrial fusion in podocytes, which at least partially mediated the effects of cAMP.
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Registered trials
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