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Introduction. Myocardial reperfusion injury answers for half of final infarct size following myocardial infarction, although no effective therapy has yet been discovered. Modulation of mitochondrial activity stands as an attractive target, as its impairment following reperfusion impairs ATP generation and henceforth turns cardiac recovery less prone to occur. HDL reduced final infarct size in different ischemia-reperfusion injury models for unknown mechanisms. Whether this effect involves mitochondrial activity modulation is unknown.

HDL preserves mitochondrial complex I activity during myocardial reperfusion injury