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Protective Effects of HDL Against Ischemia/Reperfusion Injury
Monica Gomaraschi1, Laura Calabresi1, Guido Franceschini1
1Centro E. Grossi Paoletti, Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano Milan, Italy.
Insights
Low levels of high-density lipoprotein (HDL) cholesterol negatively impact heart function after myocardial infarction. However, HDL demonstrates protective effects against ischemia/reperfusion injury, suggesting therapeutic potential.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Cell Biology
Background:
- Low plasma high-density lipoprotein (HDL) cholesterol is linked to poor prognosis post-myocardial infarction.
- Evidence suggests a detrimental effect of low HDL on post-ischemic myocardial function.
Purpose of the Study:
- To investigate the protective role of HDL in myocardial ischemia/reperfusion (I/R) injury.
- To explore the potential of HDL as a therapeutic agent for acute coronary syndromes.
Main Methods:
- Experiments utilizing ex vivo and in vivo models of myocardial I/R injury.
- Assessment of HDL's effects on coronary endothelial cells, white blood cells, and cardiomyocytes.
Main Results:
- HDL administration before ischemia or at reperfusion preserves cardiac function.
- HDL mitigates I/R injury in cardiac and other tissues like the brain and hind limb.
- HDL exerts protective mechanisms including limiting endothelial permeability, reducing inflammatory cell infiltration, and preventing cardiomyocyte apoptosis.
Conclusions:
- HDL possesses significant cardioprotective properties against I/R injury.
- Synthetic HDL retains cardioprotective activity, indicating its potential as an adjunctive therapy.
- HDL-based therapies may improve outcomes for patients with acute coronary syndromes or undergoing coronary procedures.
Abstract:
Several lines of evidence suggest that, besides being a strong independent predictor of the occurrence of primary coronary events, a low plasma high density lipoprotein (HDL) cholesterol level is also associated with short- and long-term unfavorable prognosis in patients, who have recovered from a myocardial infarction, suggesting a direct detrimental effect of low HDL on post-ischemic myocardial function. Experiments performed in ex vivo and in vivo models of myocardial ischemia/reperfusion (I/R) injury have clearly shown that HDL are able to preserve cardiac function when given before ischemia or at reperfusion; the protective effects of HDL against I/R injury have been also confirmed in other tissues and organs, as brain and hind limb. HDL were shown to act on coronary endothelial cells, by limiting the increase of endothelium permeability and promoting vasodilation and neoangiogenesis, on white blood cells, by reducing their infiltration into the ischemic tissue and the release of pro-inflammatory and matrix-degrading molecules, and on cardiomyocytes, by preventing the activation of the apoptotic cascade. Synthetic HDL retains the cardioprotective activity of plasma-derived HDL and may become a useful adjunctive therapy to improve clinical outcomes in patients with acute coronary syndromes or undergoing coronary procedures.
