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Another identified mechanism supporting the protective role of GLP-1 against myocardial ischemia/reperfusion injury is the reduction of cardiomyocyte apoptosis, as evidenced by the phosphorylation and inactivation of the pro-apoptotic peptide BAD in GLP-1-treated rat hearts (Bose et al

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Crosstalk between nuclear glucose-regulated protein 78 and Tumor Protein 53 contributes to the lipopolysaccharide aggravated apoptosis of endoplasmic reticulum stress-responsive porcine intestinal epithelial cells