High-Density Lipoprotein and Heart Failure.

Rev Cardiovasc Med

Department of Cardiology, the Second Hospital of Shandong University, 250033 Jinan, Shandong, China.

Published: November 2023

AI Article Synopsis

  • HDL is well-known for its protective effects against atherosclerosis, but its role in heart failure (HF) is still unclear and debated.
  • * Research suggests that HDL may help protect the heart through its antioxidant, anti-inflammatory, and endothelial functions, with high levels of HDL-C linked to lower instances of HF.
  • * The primary protein in HDL, Apo A-I, and the enzyme PON-1 are key components in mediating HDL's protective effects, potentially influencing the progression of heart failure.

Article Abstract

The protective effect of high-density lipoprotein (HDL) on atherosclerosis is well known, and its mechanisms of action has been extensively studied. However, the impact of HDL on heart failure and its mechanisms are still controversial or unknown. The cardioprotective role of HDL may be reflected in its antioxidant, anti-inflammatory, anti-apoptotic, and endothelial function protection. In epidemiological studies, high-density lipoprotein cholesterol (HDL-C) levels have been negatively associated with heart failure (HF). The major protein component of HDL-C is apolipoprotein (Apo) A-I, while paraoxonase-1 (PON-1) is an essential mediator for many protective functions of HDL, and HDL may act through components like (Apo) A-I or PON-1 to delay heart failure progress. HDL can slow heart failure disease progression through parts like (Apo) A-I or PON-1. The potential causality between HDL and heart failure, the role of HDL in the pathogenesis of HF, and its interaction with C-reactive protein (CRP), triglycerides (TG), and monocytes in the process of heart failure have been briefly summarized and discussed in this article. HDL plays an important role in the pathogenesis, progression and treatment of HF.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11272862PMC
http://dx.doi.org/10.31083/j.rcm2411321DOI Listing

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