ELOVL2 encodes an endoplasmic reticulum-bound fatty acid elongase that catalyzes the rate-limiting first step of long-chain fatty acid elongation, adding two carbons per cycle to synthesize very long-chain polyunsaturated fatty acids (VLC-PUFAs), particularly docosahexaenoic acid (DHA) precursors 1. The enzyme shows substrate specificity toward polyunsaturated acyl-CoA, with highest activity toward arachidonic acid 2. ELOVL2 function is critical for maintaining retinal lipid homeostasis; mice with reduced ELOVL2 activity exhibit impaired contrast sensitivity and delayed dark adaptation, while VLC-PUFA supplementation reverses age-related vision decline 1. ELOVL2 methylation status serves as a robust epigenetic aging marker, correlating strongly with chr6 age 34. Functionally, ELOVL2 deficiency increases endoplasmic reticulum stress and mitochondrial dysfunction, accelerating aging phenotypes and age-related macular degeneration in retinal epithelial cells 3. In pancreatic beta cells, ELOVL2-derived DHA protects against glucolipotoxicity-induced apoptosis through CPT1-dependent fatty acid oxidation 2. Clinically, ELOVL2 variants associate with autism spectrum disorder susceptibility and intermediate age-related macular degeneration in human populations 51. These findings position ELOVL2 as a key metabolic-epigenetic node linking lipid homeostasis to age-related disease prevention.