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[DOI] [PMC free article] [PubMed] [Google Scholar] 52.Verde C., Giordano D., Bruno S

In diabetes, HFpEF is predominantly driven by coronary microvascular disease/dysfunction, systemic inflammation, as well as cardiovascular autonomic dysfunction (which is very specific to diabetes) and a deficient heart oxidative metabolism, all leading to remodeling of the heart and increased stiffness, while HFrEF is predominantly driven by adverse remodeling secondary to accelerated atherosclerotic CVD (ASCVD)

The oxidation of specific tyrosine and methionine residues in apoA-I contributes to its loss of activity (Shao, 2012)

CD36/fatty acid translocase (FAT), highly expressed in the proximal intestine, mediates long-chain fatty acid uptake and is dynamically regulated by post-translational modifications such as palmitoylation, thereby influencing lipid flux toward portomicron assembly (5658)