ArticleCell death & disease2018
Apelin inhibited epithelial-mesenchymal transition of podocytes in diabetic mice through downregulating immunoproteasome subunits β5i.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- PTBP3 promotes diabetic nephropathy via Smad3-dependent podocyte-mesenchymal transition.Molecular biology reports · 2026Article
- 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
- The role of immunoproteasome in diabetes and diabetes-related complications.Genes & diseases · 2026Review
- Review
- Apelin/APJ alleviates diabetic nephropathy by improving glomerular endothelial cells dysfunction via SIRT3‑KLF15.Molecular medicine reports · 2025Article
- Expression of apelin‑13 and its negative correlation with TGF‑β1 in patients with diabetic kidney disease.Experimental and therapeutic medicine · 2024Article
- Btg2 Promotes Focal Segmental Glomerulosclerosis via Smad3-Dependent Podocyte-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Elabela inhibits TRAF1/NF-κB induced oxidative DNA damage to promote diabetic foot ulcer wound healing.iScience · 2023Article
- Immunoproteasome subunit β5i promotes perifascicular muscle atrophy in dermatomyositis by upregulating RIG-I.RMD open · 2023Article
- Kunxian capsule alleviates podocyte injury and proteinuria by inactivating β-catenin in db/db mice.Frontiers in medicine · 2023Article
- The Interaction of Apelin and FGFR1 Ameliorated the Kidney Fibrosis through Suppression of TGFOxidative medicine and cellular longevity · 2023Article
- The Role of Apelin-APJ System in Diabetes and Obesity.Frontiers in endocrinology · 2022Review
- Paeoniflorin directly binds to TNFR1 to regulate podocyte necroptosis in diabetic kidney disease.Frontiers in pharmacology · 2022Article
- Apelin/APJ relieve diabetic cardiomyopathy by reducing microvascular dysfunction.The Journal of endocrinology · 2021Article
- PPARγ Mediates the Anti-Epithelial-Mesenchymal Transition Effects of FGF1Frontiers in pharmacology · 2021Article
- Human ucMSCs seeded in a decellularized kidney scaffold attenuate renal fibrosis by reducing epithelial-mesenchymal transition via the TGF-β/Smad signaling pathway.Pediatric research · 2020Article
- Neuropilin 1 modulates TGF‑β1‑induced epithelial‑mesenchymal transition in non‑small cell lung cancer.International journal of oncology · 2020Observational
- Roles of the Hepatic Endocannabinoid and Apelin Systems in the Pathogenesis of Liver Fibrosis.Cells · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-mesenchymal transition (EMT) of podocytes had been reported to be involved in the glomerular fibrosis in diabetic kidney diseases, which was regulated by TGFβ and NFκB pathways. And apelin, an adipokine which is upregulated in diabetic kidney diseases, was reported to be negatively correlated to TGFβ in polycystic kidney disease and attenuate EMT in renal tubular cells. Therefore, it is hypothesized that apelin might inhibit the EMT of podocytes through downregulating the expression and activation of TGFβ/Smad pathway in diabetic kidney diseases. The results showed that apelin in glomeruli of diabetic mice were increased and exogenous apelin inhibited the EMT of podocytes in diabetic mice, which were accompanied with the decreased expression of proteasome subunits β5i. The results from β5iKO mice confirmed that the inhibiting effects of apelin on EMT of podocytes in diabetic mice were dependent on β5i. The results from culture podocytes showed that apelin decreased the degradation of pIκB and promoted the translocation of IκB into nucleus through decreasing the expression of β5i, which would inhibit the promoting effects of NFκB on expression of TGFβ and followed by decreased activation of Smad pathway and EMT in podocytes. In conclusion, apelin might act as an EMT suppressor for podocytes to decrease the process of glomerular fibrosis in diabetic mice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.