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The activation of these events leads to increased vasoconstriction and atherosclerosis, ultimately promoting a pro-thrombotic state ( 2 ), and down regulation of endothelioum-dependent hyperpolarization (EDH) and factors that cause contraction such as thromboxane A 2 (TxA 2 ) and upregulation of endothelin-1 (ET-1)

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Protein Cell 15, 642660

139 Molecular biophysics provides valuable insights into the underlying mechanisms of ACL damage, including the role of collagen degradation, mechanotransduction pathways, MMP activity, oxidative stress, and mechanobiology