Figure 4.

Schematic summary of a causal link and potential mechanisms of branched-chain amino acids (BCAAs) in cardiovascular disease (CVD). High circulating BCAA levels may influence CAD and subsequent plaque rupture events via two distinct pathways: glucose metabolism disorder (as shown by PPM1K and TRMT61A) through processes leading to chronic vulnerability to CAD and neuroendocrine dysregulation (as shown by CBLN1, MRPL33, and C2orf16) affecting hemodynamic factors and platelets through neuroendocrine factors, which in turn affect subsequent plaque rupture and thrombosis in CAD, triggering ischemic events. CAD, coronary artery disease. BCAA, branched-chain amino acids. Figure created with BioRender (biorender.com, accessed on 24 February 2023).