ArticleInternational journal of molecular medicine2019
Connexin 43‑autophagy loop in the podocyte injury of diabetic nephropathy.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Connexins in metabolic control: linking brain cellular communication to systemic homeostasis.Life medicine · 2026Review
- Connexin 43 and Pannexin 1 in Renal Cell Populations in Diabetic Kidney Disease.International journal of molecular sciences · 2026Article
- [Inhibition of miR-30d-5p promotes mitochondrial autophagy and alleviates high glucose-induced injury in podocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
- Repetitive transcranial magnetic stimulation promotes motor function recovery in mice after spinal cord injury via regulation of the Cx43-autophagy loop.Journal of orthopaedic surgery and research · 2024Article
- Small interfering RNA (siRNA) as a potential gene silencing strategy for diabetes and associated complications: challenges and future perspectives.Journal of diabetes and metabolic disorders · 2024Review
- Protective effect of the tunneling nanotube-TNFAIP2/M-sec system on podocyte autophagy in diabetic nephropathy.Autophagy · 2023Article
- Expression profiles of tRNA‑derived fragments in high glucose‑treated tubular epithelial cells.Experimental and therapeutic medicine · 2023Article
- Modes of podocyte death in diabetic kidney disease: an update.Journal of nephrology · 2022Review
- Rapamycin attenuated podocyte apoptosis via upregulation of nestin in Ang II-induced podocyte injury.Molecular biology reports · 2022Article
- Connexin 43: A Target for the Treatment of Inflammation in Secondary Complications of the Kidney and Eye in Diabetes.International journal of molecular sciences · 2022Review
- Article
- Relationship between lysosomal dyshomeostasis and progression of diabetic kidney disease.Cell death & disease · 2021Review
- Plant Polyphenols for Aging Health: Implication from Their Autophagy Modulating Properties in Age-Associated Diseases.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Podocytes and microRNA-30/Cx43 axis in diabetic nephropathy.Annals of translational medicine · 2021Article
- New insights into diabetes mellitus and its complications: a narrative review.Annals of translational medicine · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The reduction of podocyte injury is a key strategy in controlling proteinuria, which is the main early clinical manifestation of diabetic nephropathy (DN). Impaired autophagic flux is the primary mechanism responsible for podocyte injury in DN. The aim of the present study was to elucidate the effect of connexin 43 (Cx43) on impaired autophagic flux in podocyte injury and to explore its molecular mechanism of action in DN. Sprague‑Dawley rats were administered streptozocin (STZ) to construct a DN animal model. Podocytes were incubated in media containing either buffer or high glucose (HG; 30 mM) for variable time periods. The podocytes were then examined and the mechanism of injury was investigated using an Annexin V/PI assay, immunofluorescence staining, western blotting, and RNA interference. In vivo, STZ‑induced DN rats with or without Cx43 knockdown were established to observe the role of Cx43 in autophagic flux and podocyte injury. We observed that HG induced podocyte injury, accompanied by increases in Cx43 expression and impaired autophagic flux, as evidenced by the accumulation of LC3II/LC3I and p62. Interestingly, the silencing of Cx43 expression ameliorated autophagic flux impairment and reduced podocyte injury via suppression of the mammalian target of rapamycin pathway. Furthermore, impaired autophagic flux also blocked the degradation of Cx43. In vitro studies indicated that higher numbers of Annexin V/PI‑positive podocytes, impaired autophagic flux and increased Cx43 expression were observed in HG‑induced podocyte injury relative to the control group. The pathogenic effect of Cx43 on impaired autophagic flux and podocyte injury was also confirmed by Cx43 knockdown. The present study provided preliminary evidence indicating that the interdependence of Cx43 and impaired autophagic flux represents a novel mechanism of podocyte injury in DN. Hence, the Cx43‑autophagy loop is a potentially relevant therapeutic target for the treatment of DN.
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