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Endoplasmic reticulum stress‐mediated autophagy protects against lipopolysaccharide‐induced apoptosis in HL‐1 cardiomyocytes

What is the central question of this study? Cardiac dysfunction in sepsis is associated with apoptosis of cardiomyocytes. Is endoplasmic reticulum (ER) stress induced in lipopolysaccharide (LPS)‐treated cardiomyocytes? Does ER stress‐induced autophagy protect against LPS‐induced apoptosis of cardiomyocytes? What is the mechanism in detail? What is the main finding and its importance? Our results indicate that ER stress is activated and mediates autophagy in LPS‐treated murine atrium‐derived cardiac HL‐1 cells. Protein kinase regulated by RNA‐like ER‐associated kinase (PERK), one arm of ER stress, is involved in protecting against LPS‐induced apoptosis of HL‐1 cells by promotion of autophagy.