Lipid Droplet-Associated Proteins in Cardiomyopathy

Abstract

<b><i>Background:</i></b> The heart requires a high rate of fatty-acid oxidation (FAO) to meet its energy needs. Neutral lipids are the main source of energy for the heart and are stored in lipid droplets (LDs), which are cytosolic organelles that primarily serve to store neutral lipids and regulate cellular lipid metabolism. LD-associated proteins (LDAPs) are proteins either located on the surface of the LDs or reside in the cytosol and contribute to lipid metabolism. Therefore, abnormal cardiac lipid accumulation or FAO can alter the redox state of the heart, resulting in cardiomyopathy, a group of diseases that negatively affect the myocardial function, thereby leading to heart failure and even cardiac death. <b><i>Summary:</i></b> LDs, along with LDAPs, are pivotal for modulating heart lipid homeostasis. The proper cardiac development and the maintenance of its normal function depend largely on lipid homeostasis regulated by LDs and LDAPs. Overexpression or deletion of specific LDAPs can trigger myocardial dysfunction and may contribute to the development of cardiomyopathy. Extensive connections and interactions may also exist between LDAPs. <b><i>Key Message:</i></b> In this review, the various mechanisms involved in LDAP-mediated regulation of lipid metabolism, the association between cardiac development and lipid metabolism, as well as the role of LDAPs in cardiomyopathy progression are discussed.

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