Biomolecular mechanisms of cardiac amyloidosis and its cardiovascular pathological basis

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Cardiac amyloidosis (CA) is primarily caused by transthyretin (ATTR) or immunoglobulin light chain (AL) amyloid deposition in the heart.
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Myocardial injury in CA involves not only fibril accumulation but also soluble toxic intermediates and immune-inflammatory activation.
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ATTR and AL amyloidosis differ in their upstream drivers and the contributions of deposition-dependent versus soluble toxicity-mediated injury.
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Emerging evidence highlights the role of immune-inflammatory signaling and proteostasis stress in the progression of cardiac amyloidosis.
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A better understanding of the molecular pathways in CA may enhance diagnosis, risk stratification, and development of targeted therapies.

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