ArticleCell death & disease2017
Apelin involved in progression of diabetic nephropathy by inhibiting autophagy in podocytes.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 74 citations in OpenAlex.
- Research trends and frontiers of the Apelin system in kidney diseases: a multi-database bibliometric analysis and cross-validation study.International urology and nephrology · 2026Review
- Context‑dependent duality of the apelin/elabela‑APJ system in diabetes and its complications (Review).International journal of molecular medicine · 2026Review
- International Union of Basic and Clinical Pharmacology. CXXI. Apelin receptor pharmacology in the human cardiovascular system and emerging clinical applications.Pharmacological reviews · 2026Review
- Role of Apelin in Type II Diabetes Mellitus.Cureus · 2026Article
- Review
- The Apelinergic System in Kidney Disease: Novel Perspectives.International journal of molecular sciences · 2025Review
- Diagnostic value of the correlation between urinary MDM2 and podocyte mitotic catastrophe in diabetic kidney disease.Diabetology & metabolic syndrome · 2025Article
- SIRT1/PGC-1α-mediated mitophagy participates the improvement roles of BMAL1 in podocytes injury in diabetic nephropathy: evidences from in vitro experiments.European journal of medical research · 2025Article
- Insights into the effects of apelin-13 on renal function and NHE3 activity following ischemia/reperfusion-induced acute kidney injury.Frontiers in physiology · 2025Article
- Exploring the Molecular Modalities in the Pathogenesis of Diabetic Kidney Disease with a Focus on the Potential Therapeutic Implications.Biomedicines · 2024Review
- Effects of apelin on neonatal brain neurogenesis in L-NAME-induced maternal preeclampsia.Scientific reports · 2024Article
- Apelin-13 administration allows for norepinephrine sparing in a rat model of cecal ligation and puncture-induced septic shock.Intensive care medicine experimental · 2024Article
- STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress.Toxicology research · 2024Article
- Quercetin prevents kidney against diabetes mellitus (type 1) in rats by inhibiting TGF-β/apelin gene expression.Molecular biology reports · 2024Article
- Expression of apelin‑13 and its negative correlation with TGF‑β1 in patients with diabetic kidney disease.Experimental and therapeutic medicine · 2024Article
- Downregulation of TRPC6 regulates ERK1/2 to prevent sublytic C5b‑9 complement complex‑induced podocyte injury through activating autophagy.Experimental and therapeutic medicine · 2023Article
- Acteoside protects podocyte against apoptosis through regulating AKT/GSK-3β signaling pathway in db/db mice.BMC endocrine disorders · 2023Article
- Glomerular filtration rate in patients with type 2 diabetes mellitus: is serum isthmin-1 level a possible link?BMJ open diabetes research & care · 2023Article
- GSDME-dependent pyroptosis signaling pathway in diabetic nephropathy.Cell death discovery · 2023Article
- The Interaction of Apelin and FGFR1 Ameliorated the Kidney Fibrosis through Suppression of TGFOxidative medicine and cellular longevity · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte autophagy dysfunction has been reported to be responsible for the progression of diabetic nephropathy (DN), however, the factors contributed to autophagy dysfunction in type 2 diabetes are not fully understood. Among promoting factors in DN, an adipokine, apelin, had been showed to trigger podocyte dysfunction. Therefore, it is hypothesized that apelin, which is increased in plasma in type 2 diabetes, lead to podocyte apoptosis through inhibiting podocyte autophagy, which resulted in podocyte dysfunction followed by DN. KkAy mice (diabetic mice) and cultured podocytes (MPC5 cells and native podocytes) were treated with high glucose (HG) and apelin or its antagonist F13A. Renal function, podocyte autophagy, podocyte apoptosis and corresponding cell signaling pathways in podocytes were detected. The results showed that apelin aggravated the renal dysfunction and foot process injuries in kkAy mice, which is positively correlated to podocyte apoptosis and negatively correlated to podocyte autophagy. Apelin induced podocyte apoptosis and inhibited podocyte autophagy in both normal glucose and HG conditions while F13A reversed these effects. Investigations by western blot found that apelin inhibits podocyte autophagy through ERK-, Akt- and mTOR-dependent pathways. In conclusion, increased apelin concentration in plasma inhibited podocyte autophagy, which would lead to podocyte apoptosis and renal dysfunction in diabetes. These effects would contribute to the progression of DN.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.