Role of high-density lipoproteins in cardioprotection and in reverse remodeling: Therapeutic implications

Bart De Geest*, Mudit Mishra

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

1 Citation (Scopus)

Abstract

Cardioprotection includes all mechanisms that contribute to preservation of the heart by reducing or even preventing myocardial damage. High-density lipoproteins (HDLs) are circulating multimolecular platforms that exert a multitude of effects on cardiomyocytes and nonmyocyte cells in the myocardium leading to preservation of cardiac structure and function. Animal intervention studies applying HDL-targeted therapies have provided consistent evidence that HDLs protect against ischemia-reperfusion injury, leading to smaller myocardial infarctions, and that HDLs attenuate infarct expansion and cardiac remodeling post-myocardial infarction. These beneficial effects of HDLs are not restricted to prevention of development of ischemic cardiomyopathy but also apply to prevention of pathological hypertrophy and adverse remodeling in the presence of diabetes or in the presence of pressure overload. Moreover, HDLs can induce reverse remodeling characterized by a reduction of cardiac hypertrophy, a decrease of myocardial fibrosis, a regression of capillary rarefaction, and a restoration of cardiac function. HDL-targeted interventions are an effective treatment for heart failure in animal models. In conclusion, whereas protective effects of HDLs on coronary arteries remain essentially unproven till now, the potential for clinical translation of HDL-targeted interventions in prevention of cardiomyopathy and in treatment of heart failure is supported by consistent evidence from animal intervention studies.

Original languageEnglish
Article number159022
JournalBiochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
Volume1866
Issue number11
DOIs
Publication statusPublished - Nov 2021

Keywords

  • Cardiac remodeling
  • Gene transfer
  • HDL
  • Heart failure
  • Infarct expansion
  • Ischemiareperfusion injury

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