ArticleWorld journal of diabetes2024
MicroRNA-630 alleviates inflammatory reactions in rats with diabetic kidney disease by targeting toll-like receptor 4.
Article in World journal of diabetes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- MicroRNA Regulation in Kidney Interstitial Fibrosis.Epigenomes · 2026Review
- MiR-509-3p Targets YAP1 to Regulate Inflammatory Cytokines Against Hyperglycemia-Induced Renal Tubular Cell Damage in Diabetic Kidney Disease.Combinatorial chemistry & high throughput screening · 2026Article
- Crosstalk between microRNAs and autophagy in adipocyte differentiation: emerging therapeutic targets for obesity.Adipocyte · 2025Review
- Pathogenesis and Therapeutic Perspectives of Tubular Injury in Diabetic Kidney Disease: An Update.Biomedicines · 2025Review
- MiR-203 improved renal cell injury in diabetic nephropathy by targeting SOCS6/SOCS7 and inhibiting JAK/STAT pathway activation.Scientific reports · 2025Article
- MicroRNA-630: A potential guardian against inflammation in diabetic kidney disease.World journal of diabetes · 2024Article
- MicroRNA-630: A promising avenue for alleviating inflammation in diabetic kidney disease.World journal of diabetes · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiabetic kidney disease (DKD) is a major complication of diabetes mellitus. Renal tubular epithelial cell (TEC) damage, which is strongly associated with the inflammatory response and mesenchymal trans-differentiation, plays a significant role in DKD; However, the precise molecular mechanism is unknown. The recently identified microRNA-630 (miR-630) has been hypothesized to be closely associated with cell migration, apoptosis, and autophagy. However, the association between miR-630 and DKD and the underlying mechanism remain unknown.
aimTo investigate how miR-630 affects TEC injury and the inflammatory response in DKD rats.
methodsStreptozotocin was administered to six-week-old male rats to create a hyperglycemic diabetic model. In the second week of modeling, the rats were divided into control, DKD, negative control of lentivirus, and miR-630 overexpression groups. After 8 wk, urine and blood samples were collected for the kidney injury assays, and renal tissues were removed for further molecular assays. The target gene for miR-630 was predicted using bioinformatics, and the association between miR-630 and toll-like receptor 4 (TLR4) was confirmed using
resultsThe expression level of miR-630 was reduced in the kidney tissue of rats with DKD (
conclusionMiR-630 may inhibit the inflammatory reaction of DKD by targeting TLR4, and has a protective effect on DKD.
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