Key result
Macrophage migration inhibitory factor deficiency in mice exacerbated starvation-induced left ventricular contractile anomalies and interrupted autophagy.
Population
Wild-type (WT) and MIF knockout mice; neonatal mouse cardiomyocytes from WT and MIF-/- mice; H9C2 cells
Comparison
Acute starvation challenge vs Wild-type mice/cells under starvation, and…
Design
Preclinical
Follow-up
48 hours (in vivo), 2 hours (in vitro)
Authors
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No immediate clinical implications; extends preclinical evidence for MIF in autophagy during cardiac stress.
Macrophage migration inhibitory factor (MIF) plays a critical permissive role in maintaining cardiac contractile function during starvation by regulating autophagy.
Xu et al. (2013) studied starvation-induced cardiac contractile dysfunction. Macrophage migration inhibitory factor (MIF) deficiency vs. Wild-type was evaluated on cardiac geometry, contractile and intracellular Ca2+ properties. Macrophage migration inhibitory factor deficiency in mice exacerbated starvation-induced left ventricular contractile anomalies and interrupted autophagy.
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