Deficiency of STING attenuated MCD-induced hepatic steatosis and fibrosis in mice. WT and STING-deficient mice (Tmem173 gt) were fed with MCD for 8 weeks to induce NASH. H&E (Figure 1A) and Masson staining (Figure 1B) revealed steatosis, ballooning, inflammation, and fibrosis in the livers of MCD-fed mice, which was attenuated by deficiency of STING. Levels of cholesterol (Figure 1C), triglyceride (Figure 1D), and hydroxyproline (a marker of fibrosis, Figure 1E) in livers and levels of ALT (Figure 1F) and aspartate aminotransferase (AST) (Figure 1G

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Background and purpose Myocardial infarction (MI) is one of the leading causes of death in China and often results in the development of heart failure. In this work, we tested the therapeutic role of Interleukin‐19 (IL‐19) in mice with MI and investigated the underlying molecular mechanism. Experimental approach Mice were subjected to MI by ligation of left anterior descending coronary artery (LAD) and treated with IL‐19 (10ng g‐1; i.p.). Key results Protein expression of IL‐19 and its receptor in myocardium were upregulated 24 hrs post‐MI in male mice. IL‐19 treatment decreased infarct and apoptosis in myocardium, accompanied by enhanced haem oxygenase‐1 (HO‐1) activities and reduced malondialdehyde (MDA) formation. Pretreatment with IL‐19 upregulated HO‐1 expression in cultured neonatal mouse ventricular myocytes and attenuated oxygen‐glucose deprivation (OGD)‐induced injuries in vitro. Furthermore, IL‐19 preserved cardiac function and improved survival of mice with MI. IL‐19 reduced inflammatory infiltrates and suppressed formation of TNF‐α, IL‐1β, and IL‐6. More importantly, IL‐19 inhibited polarization toward proinflammatory M1 macrophages and stimulated M2 macrophage polarization in myocardium of mice with MI. IL‐19 enhanced protein levels of vascular endothelial growth factor (VEGF) and promoted angiogenesis in myocardium of mice with MI. In addition, IL‐19 treatment increased DNA‐binding of the transcription factor STAT3 in myocardium of mice with MI. Conclusions and Implications Treatment with exogenous IL‐19 attenuated acute ischemic injury and improved survival of mice with MI. The mechanisms underlying these effects involved induction of HO‐1, M2 macrophage polarization, angiogenesis, and STAT3 activation.