New mechanisms for metabolism to regulate thrombosis and new targets for treatment have been revealed

The Liu Junling Group of Shanghai Jiaoxuan University School of Medicine, in collaboration with Sun Haipeng, for the first time closely linked branch chain amino acid (BCAA) metabolism with platelet function and thrombosis risk, revealing a new mechanism for BCAA metabolism to regulate platelet activity and thrombosis. The results were published in Blood Circulation on March 23.
Because ingestion of BCAA is widely used in professional athletes and sports people to increase muscle nutrients, BCAA injections are used in the treatment of hepatic encephalopathy, BCAA metabolites α-ketoa acid is used in the treatment of chronic kidney disease, the results of this study suggest that clinical application of BCAA and its downstream metabolites may be potentially hydrant risk. In addition, the study suggests that BCAA may be a new way to treat and prevent thrombosis by breaking down metabolic pathways or controlling BCAA intake in the diet.
plateplates are the main participants in thrombosis and are important target cells for cardiovascular disease treatment. Studies have shown that plateplates in people with metabolic syndrome or type 2 diabetes are usually highly active, possibly due to increased oxidation of LDL and late glycosylated end products, lower insulin levels, and plateboard mitochondrial dysfunction. Recent studies have shown that branch chain amino acid (BCAA) metabolic disorders caused by metabolic syndrome are closely related to cardiovascular disease, but the relationship between BCAA metabolic disorders and platelet activity and susceptible tendencies is not clear.
, by analyzing clinical samples of patients with type 2 diabetes, the researchers found that BCAA levels in patients' plateplates and key gene expression levels that regulate BCAA's decomposition metabolism were significantly associated with high plateboard reactiveness in patients. Reducing BCAA intake significantly reduced plate plate activity in mice with the leptin gene's pure mutation ob/ob. These results suggest that high plateboard activity in patients with metabolic syndrome or type 2 diabetes may be due to plateboard BCAA metabolic disorders. Further studies have found that oral BCAA significantly promotes plate activity in humans and mice, and promotes the formation of aortic and micro arterial thrombosis in mice. Proteophosphatase 2Cm (PP2Cm) can specifically dephosphatize branch α-ketonate dehydrogenase, thereby activating BCAA decomposition metabolism.
researchers used acrylamide proteomics and immunoprinting experiments to find that BCAA metabolism significantly increased the acrylamide modification of Tropomodulin-3 (TMOD3) K255 bits. This suggests that TMOD3 K255-bit acrylamide modification can regulate the reconstruction of the cytostebrae mediated by the integrator alpha IIb beta3, which may be the main mechanism for BCAA metabolism, especially proline metabolism, to regulate plate activity and thrombosis. (Source: Huang Xin Yangjing, China Science Journal)
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