Adiponectin alleviates the symptoms of ischemic renal disease by inhibiting renal cell apoptosis

Ischemic renal disease (IRD) can cause kidney damage and eventually lead to end-stage renal disease. Adiponectin (APN), a recently discovered collagen-like protein secreted by adipose tissues, plays an important role in regulating energy metabolism and inflammation. This study aimed to explore the specific mechanism by which APN affects IRD. Main

We cultured human renal tubular epithelial cells (HK-2) and created a mouse model of IRD to detect apoptosis-related indicators in vitro and in vivo. Key findings: Compared with those in the control group, the apoptosis rate and expression levels of Bax and Fas increased in the CoCl2-induced hypoxia model group. However, the expression of Bcl-2 decreased, and after the combined treatment with APN, the phenomenon mentioned above was reversed. Moreover, studies have found that stanniocalcin-1 (STC-1) and uncoupling protein3 (UCP3) are also involved in the protective effect of APN. Additionally, we found that the glomeruli of the mice were significantly enlarged after the APN gene was knocked out; furthermore, the number of collagen fibers in the renal tubules, as well as the expression of the corresponding fibrogenic factors, increased significantly. More importantly, after the knockout of the APN gene, the expression of the hypoxia-inducible factors HIF-1α and HIF-1β and the apoptotic rate of renal tissue cells also increased. Significance: These

These results indicate that APN can alleviate the symptoms of IRD by inhibiting renal cell apoptosis. Thus, in the future, APN may be a new target for the treatment of IRD. Chemical compounds: Cobalt chloride (PubChem CID: 24643).