<p>Cardiac amyloidosis caused by amyloid light chain proteins is a life-threatening manifestation of systemic amyloid light chain amyloidosis, yet it remains underrecognized. This review explores the pathogenic mechanisms underlying cardiac involvement in amyloid light chain amyloidosis, focusing on two key pathways: the physical disruption from extracellular amyloid deposition and direct cardiotoxicity from circulating light chains, which induce oxidative stress, mitochondrial dysfunction, and apoptosis. Emerging therapies, including cellular immunotherapies such as chimeric antigen receptor T cells and bispecific antibodies, plasma cell-directed agents, and strategies that promote amyloid fibril removal or restore cardiomyocyte function are also evaluated. Despite advances, challenges persist in managing toxicities, accelerating amyloid clearance, and validating treatments in broader populations. Future efforts should prioritize early diagnosis, optimized combination therapies, mass spectrometry-driven drug discovery, and the development of reliable human <i>in vitro</i> and animal models to better recapitulate disease mechanisms and facilitate therapeutic development.</p>