Abstract
Cardiac involvement has a profound effect on the prognosis of patients with systemic amyloidosis. Therapeutic methods for suppressing the production of causative proteins have been developed for ATTR amyloidosis and AL amyloidosis, which show cardiac involvement, and the prognosis has been improved. However, a method for removing deposited amyloid has not been established. Methods for reducing cytotoxicity caused by amyloid deposition and amyloid precursor protein to protect cardiovascular cells are also needed. In this review, we outline the molecular mechanisms and treatments of cardiac amyloidosis.
Highlights
Amyloidosis is a general term for diseases in which misfolded proteins form amyloid fibrils that are rich in a unique β-sheet structure and the amyloid fibrils are deposited in various organs throughout the body and cause organ dysfunction [1]
We describe the molecular mechanisms and treatments of cardiac amyloidosis
Organ damage and prognosis depend on the cumulative deposition of amyloid fibrils and on the type of fibrils deposited. This has been demonstrated by the worse prognosis for cardiac amyloidosis in AL fibrils than in ATTR fibrils, despite high cumulative fibril deposition in ATTR amyloidosis [18]
Summary
Amyloidosis is a general term for diseases in which misfolded proteins form amyloid fibrils that are rich in a unique β-sheet structure and the amyloid fibrils are deposited in various organs throughout the body and cause organ dysfunction [1]. The causative proteins of these amyloidosis forms have been identified and the mechanisms of amyloid aggregation have been elucidated, and promising treatments have emerged with the evolution of biotechnology [5,6,7,8,9,10]. There are still unclear points, such as the cardiotropic mechanisms and amyloid removal mechanisms, and it is thought that elucidation of these points will lead to better treatment. We describe the molecular mechanisms and treatments of cardiac amyloidosis
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