ArticleAnnals of translational medicine2020
MicroRNA-30/Cx43 axis contributes to podocyte injury by regulating ER stress in diabetic nephropathy.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Propafenone-mediated gap junctional uncoupling results from aberrant connexin-43 trafficking.Pharmacological reports : PR · 2026Article
- Erratum: MicroRNA-30/Cx43 axis contributes to podocyte injury by regulating ER stress in diabetic nephropathy.Annals of translational medicine · 2025Article
- Long noncoding RNA protein-disulfide isomerase-associated 3 regulated high glucose-induced podocyte apoptosis in diabetic nephropathy through targeting miR-139-3p.World journal of diabetes · 2024Article
- The pathological role of damaged organelles in renal tubular epithelial cells in the progression of acute kidney injury.Cell death discovery · 2022Review
- Urinary Extracellular Vesicles and Their miRNA Cargo in Patients with Fabry Nephropathy.Genes · 2021Article
- Podocytes and microRNA-30/Cx43 axis in diabetic nephropathy.Annals of translational medicine · 2021Article
- MicroRNAs for podocyte injury in diabetic nephropathy.Annals of translational medicine · 2021Article
- Intercellular transmission of endoplasmic reticulum stress through gap junction targeted by microRNAs as a key step of diabetic kidney diseases?Annals of translational medicine · 2021Article
- Article
- New insights into diabetes mellitus and its complications: a narrative review.Annals of translational medicine · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe microRNA-30 family plays a critical role in the pathogenesis of podocyte injury. Cx43 plays an essential role in intercellular communication, which is essential for coordinated kidney function. This study was conducted to explore the function of microRNA-30s/Cx43 in podocyte injury in diabetic nephropathy (DN), both
methodsSD rats were given streptozotocin (STZ) injections to induce DN. Podocytes were incubated in the medium in the presence or absence of high glucose (HG). The effects of the microRNA-30/Cx43 axis on DN and its underlying mechanisms were investigated by TUNEL assay, PAS, immunohistochemical staining, immunofluorescence staining, Western blot, RT-qPCR, RNA interference, and luciferase reporter assay. Podocytes were transfected with microRNA-30 family mimics, microRNA-30 family inhibitors, Cx43 siRNA, and negative controls to detect the effect of the microRNA-30/Cx43 axis. MicroRNA-30 family mimic AAVs, and microRNA-30 family inhibitor AAVs applied to regulate microRNA-30 family expression in the kidneys of the STZ-induced DN model rats to reveal the underlying mechanisms of the microRNA-30/Cx43 axis in DN.
resultsMicroRNA-30 family member expression was downregulated in HG-treated podocytes and the glomeruli of STZ-induced DN rats. Luciferase reporter assays confirmed Cx43 is a directed target of microRNA-30s. The overexpression of microRNA-30 family members attenuated the HG-induced podocyte injury and protected against podocyte apoptosis and endoplasmic reticulum stress (ERS) both
conclusionsThe overexpression of microRNA-30 family members prevents HG-induced podocyte injury and attenuates ERS by modulating Cx43 expression. The microRNA-30/Cx43/ERS axis might be a potential therapeutic target to treat DN.
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