Proteomic Analysis on Myocardial Injury Induced by Hyperuricemia Rats

Hyperuricemia (HUA) has been confirmed to be closely associated with the occurrence and progression of cardiovascular diseases; however, the specific molecular mechanisms through which it induces myocardial injury remain to be fully elucidated. This study aimed to investigate the cardiotoxic effects of HUA and explore associated proteomic alterations by establishing a HUA rat model. Myocardial injury was assessed by measuring serum levels of uric acid (UA), creatine kinase (CK), creatine kinase isoenzyme MB (CK-MB), and cardiac troponin T (cTnT). Differential protein expression profiles were analyzed using proteomic techniques. The results showed significantly elevated levels of UA, CK, CK-MB, and cTnT in the model group. A total of 40 differentially expressed proteins were identified, including 11 up-regulated and 30 down-regulated proteins, such as CCDC88C, LPIN1, and SDHD, which are associated with inflammatory response, oxidative stress, and mitochondrial dysfunction. GO functional analysis indicated that these proteins are involved in biological processes including myocardial hypertrophy, contraction, and fibrosis. This study reveals potential mechanisms by which HUA may contribute to myocardial injury at the protein level, providing a theoretical basis for further research.