MiR‐325‐3p inhibits renal inflammation and fibrosis by targeting CCL19 in diabetic nephropathy

Diabetic nephropathy (DN), a common cardiovascular disease, has been a global health threat. MicroRNAs (miRNAs) have been proposed to frequently participate in the occurrence and development of DN, however, the role of miR‐325‐3p in DN remains uncharacterized. Our research aimed to explore the function and mechanism of miR‐325‐3p in DN. Bioinformatics analysis (Targetscan, http://www.targetscan.org) and a wide range of experiments including RT‐qPCR, CCK‐8 assay, western blot, luciferase reporter assay, RNA immunoprecipitation (RIP) assays, urine protein and blood glucose assays, histology analysis and morphometric analysis were used to explore the function and mechanism of miR‐325‐3p and C‐C motif chemokine ligand 19 (CCL19). CCL19 could facilitate the progression of DN by inhibiting cell viability and promoting inflammation and fibrosis in HK‐2 and HMC cells. In addition, CCL19 was confirmed to be targeted and negatively regulated by miR‐325‐3p. Rescue assays validated that the impacts of miR‐325‐3p mimics on the viability, inflammation and fibrosis of HK‐2 and HMC cells were recovered by CCL19 overexpression. To sum up, miR‐325‐3p inhibits renal inflammation and fibrosis by targeting CCL19 in a DN cell model and mice model, implying miR‐325‐3p as a possible therapeutic target for DN treatment. MiR‐325‐3p promotes cell viability and inhibits inflammation response as well as fibrosis by targeting CCL19 in high glucose induced HK‐2 and HMC cells, indicating miR‐325‐3p as a potential molecular marker for diabetic nephropathy treatment.