apoC1

Apolipoprotein C-I (apoC-I) is a small exchangeable apolipoprotein primarily associated with high-density lipoproteins (HDL) and triglyceride-rich lipoproteins, where it functions as a key regulator of lipoprotein metabolism and lipid transport^[1][2]. Mechanistically, apoC-I modulates several pathways that control plasma lipid homeostasis by inhibiting lipoprotein lipase (LPL)-mediated triglyceride hydrolysis, reducing the interaction of very-low-density lipoproteins (VLDL) with lipoprotein receptors, and suppressing cholesteryl ester transfer protein (CETP) activity, thereby influencing both triglyceride and cholesterol flux between lipoprotein particles^[1][2][3]. Through these actions, apoC-I contributes to the regulation of HDL remodeling, VLDL clearance, and overall lipid distribution in circulation^[1][3]. Beyond lipid metabolism, apoC-I has been implicated in inflammatory and immune processes, linking dyslipidemia with cardiovascular and metabolic disease pathogenesis^[2][4]. Experimental studies further demonstrate that apoC-I can modulate host responses to bacterial lipopolysaccharide and influence inflammatory signaling in disease-relevant models^[4]. Compared with related apolipoprotein C family members, apoC-I is distinguished by its potent inhibition of CETP and its ability to interfere with apolipoprotein E-dependent lipoprotein receptor interactions, highlighting a unique regulatory role in lipoprotein trafficking^[2][3]. Because of these properties, apoC-I is widely used as a mechanistic target in studies of hypertriglyceridemia, atherosclerosis, diabetes-associated lipid abnormalities, and lipoprotein metabolism, while genetic and transgenic models continue to provide valuable platforms for investigating its biological functions and therapeutic relevance^[1][2][5].

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