CD74 knockout protects against LPS‐induced myocardial contractile dysfunction through AMPK‐Skp2‐SUV39H1 ‐mediated demethylation of BCLB

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Mitochondrial ALDH2 protects against lipopolysaccharide-induced myocardial contractile dysfunction by suppression of ER stress and autophagy

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CD74 knockout attenuates alcohol intake-induced cardiac dysfunction through AMPK-Skp2-mediated regulation of autophagy

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ALDH2 protects against high fat diet-induced obesity cardiomyopathy and defective autophagy: role of CaM kinase II, histone H3K9 methyltransferase SUV39H, Sirt1, and PGC-1α deacetylation

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Ablation of toll-like receptor 4 attenuates aging-induced myocardial remodeling and contractile dysfunction through NCoRI-HDAC1-mediated regulation of autophagy

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Macrophage migration inhibitory factor knockout attenuates endotoxin-induced cardiac dysfunction in mice

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Macrophage migration inhibitory factor mediates metabolic dysfunction induced by atypical antipsychotic therapy

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Selection Pressure Pathways and Mechanisms of Resistance to the Demethylation Inhibitor-Difenoconazole in Penicillium expansum

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Ablation of Akt2 prevents paraquat-induced myocardial mitochondrial injury and contractile dysfunction: Role of Nrf2

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The histone H3K9 methyltransferase SUV39H links SIRT1 repression to myocardial infarction

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The biological function and significance of CD74 in immune diseases

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Permissive role of AMPK and autophagy in adiponectin deficiency-accentuated myocardial injury and inflammation in endotoxemia

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AMPK–SKP2–CARM1 signalling cascade in transcriptional regulation of autophagy

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Macrophage Migration Inhibitory Factor (MIF) Deficiency Exacerbates Aging-Induced Cardiac Remodeling and Dysfunction Despite Improved Inflammation: Role of Autophagy Regulation

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High levels of serum macrophage migration inhibitory factor and interleukin 10 are associated with a rapidly fatal outcome in patients with severe sepsis

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Macrophage migration inhibitory factor (MIF) knockout preserves cardiac homeostasis through alleviating Akt-mediated myocardial autophagy suppression in high-fat diet-induced obesity

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Ablation of Akt2 protects against lipopolysaccharide-induced cardiac dysfunction: Role of Akt ubiquitination E3 ligase TRAF6

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Myocardial Fibrosis Induced by Exposure to Subclinical Lipopolysaccharide Is Associated with Decreased miR-29c and Enhanced NOX2 Expression in Mice

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Protective role of PARK2/Parkin in sepsis-induced cardiac contractile and mitochondrial dysfunction

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Chronic Akt activation attenuated lipopolysaccharide-induced cardiac dysfunction via Akt/GSK3β-dependent inhibition of apoptosis and ER stress

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Macrophage Migration Inhibitory Factor Deletion Exacerbates Pressure Overload–Induced Cardiac Hypertrophy Through Mitigating Autophagy

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Inhibition of protein kinase C βII isoform rescues glucose toxicity-induced cardiomyocyte contractile dysfunction: Role of mitochondria

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Recurrent Exposure to Subclinical Lipopolysaccharide Increases Mortality and Induces Cardiac Fibrosis in Mice

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Macrophage migration inhibitory factor (MIF) is a critical mediator of the innate immune response to Mycobacterium tuberculosis

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The anti-apoptotic Bcl-B protein inhibits BECN1-dependent autophagic cell death

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Cardiac-specific overexpression of catalase attenuates lipopolysaccharide-induced myocardial contractile dysfunction: Role of autophagy

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Akt2 knockout preserves cardiac function in high-fat diet-induced obesity by rescuing cardiac autophagosome maturation

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Activation of Akt Rescues Endoplasmic Reticulum Stress-Impaired Murine Cardiac Contractile Function via Glycogen Synthase Kinase-3β-Mediated Suppression of Mitochondrial Permeation Pore Opening

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Aldehyde dehydrogenase-2 (ALDH2) ameliorates chronic alcohol ingestion-induced myocardial insulin resistance and endoplasmic reticulum stress

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Cardiac overexpression of metallothionein rescues cardiac contractile dysfunction and endoplasmic reticulum stress but not autophagy in sepsis

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LPS-induced autophagy is mediated by oxidative signaling in cardiomyocytes and is associated with cytoprotection

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AMP-activated protein kinase agonist dose dependently improves function and reduces apoptosis in glucotoxic β-cells without changing triglyceride levels

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