Chemerin-Like Receptor 1 Deficiency Mitigates Renal Ischemia-Reperfusion Damage via Inflammatory Pathway Modulation.

Chemerin, a recently identified adipokine, and its receptor are known to be involved in inflammatory processes. However, their roles in renal ischemia-reperfusion (IR) injury remain unclear. The present study was designed to investigate the impact of chemerin-like receptor 1 (CMKLR1) deficiency on renal IR injury. A mouse model of renal IR injury was established using both CMKLR1 knockout (Cmklr1⁻/⁻) and wild-type (WT) mice. Blood urea nitrogen (BUN) and serum creatinine (Scr) levels were measured to assess renal function. Kidney injury was evaluated through Hematoxylin and Eosin staining. Additionally, ELISA, quantitative real-time PCR, and Western blotting were used to assess biomarker expression at both the transcriptional and protein levels. Following IR injury, chemerin and CMKLR1 levels were significantly elevated in both serum and kidney tissues. A positive correlation was observed between serum chemerin and CMKLR1 levels. Moreover, increased levels of inflammatory cytokines were also positively correlated with chemerin and CMKLR1 expression. Notably, CMKLR1 deficiency resulted in reduced BUN and Scr levels, alleviated renal tissue damage, and decreased inflammatory cytokine expression in the renal IR injury model. These findings demonstrate that CMKLR1 deficiency protects against renal IR injury by modulating inflammatory responses.