Key result
In vivo, Mito Q@MMNv improved cardiac function and the inflammatory microenvironment, increasing left ventricular ejection fraction by 62% and shifting the M1/M2 ratio.
Why the study?
Reperfusion therapy for acute myocardial infarction is limited by myocardial ischemia-reperfusion injury, and current nanoplatforms cannot simultaneously target mitochondrial dysfunction in both cardiomyocytes and macrophages.
Does Mito Q@MMNv improve cardiac function and the inflammatory microenvironment in an in vivo model of myocardial ischemia-reperfusion injury?
Design
Preclinical in vivo and in vitro study
Authors
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Mitochondria-targeted nanotherapy attenuates experimental MIRI; leaves open clinical translation in reperfusion injury.
Does Mito Q@MMNv improve cardiac function and the inflammatory microenvironment in an in vivo model of myocardial ischemia-reperfusion injury?
A novel dual-targeted metabolic nanovesicle (Mito Q@MMNv) shows promise in a preclinical model for attenuating myocardial ischemia-reperfusion injury by targeting both cardiomyocytes and macrophages.
Xue et al. (2025) studied Myocardial ischemia-reperfusion injury (MIRI). Mito Q@MMNv was evaluated on Cardiac function and inflammatory microenvironment. In vivo, Mito Q@MMNv improved cardiac function and the inflammatory microenvironment, increasing left ventricular ejection fraction by 62% and shifting the M1/M2 ratio.
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