Key result
Medin amyloid drives vascular remodeling and cardiovascular disease by scaffolding other amyloid proteins.
Why the study?
Medin amyloid plays key roles in the pathogenesis of various cardiovascular diseases, but its implications for diagnosis and treatment of cardiac amyloidosis remain unclear.
Medin amyloidosis is a key pathophysiological factor in cardiovascular aging and diseases, presenting a potential future target for diagnosing and treating cardiac and vascular amyloidosis.
Medin amyloid may represent a future therapeutic target in vascular aging; leaves open whether modulating it improves clinical cardiovascular outcomes.
Medin, a 50-residue cleavage polypeptide of milk fat globule protein epidermal growth factor 8 (MFG-E8), has been deemed to play key roles in the pathogenesis of many cardiovascular diseases, including aortic amyloidosis, hypertension, atherosclerosis, aortic dissection, heart failure, and coronary artery disease. The interactions between medin and vascular cells, such as endothelial cells in intima, vascular smooth muscle cells in media, and fibroblasts in adventitia, are considered to be involved in the pathophysiological processes of the vascular remodelling that underlies cardiovascular diseases. Recent evidence has indicated that medin could also act as a scaffold to facilitate the depositions of other types of amyloid proteins, thereby inducing cardiovascular injuries.
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Wang et al. (2021) conducted a review in Cardiovascular diseases (aortic amyloidosis, hypertension, atherosclerosis, heart failure). Medin amyloid was evaluated. Medin amyloid plays a key role in the pathogenesis of vascular remodeling and cardiovascular diseases, acting as a scaffold for other amyloid proteins.
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