Hyperglycemia Induces Endoplasmic Reticulum Stress in Atrial Cardiomyocytes, and Mitofusin-2 Downregulation Prevents Mitochondrial Dysfunction and Subsequent Cell Death

<div>Central illustration. Mfn2 deficiency in this study protected cardiomyocytes against mitochondrial depolarization/reactive oxygen species (ROS) and programmed cell death, improving atrial remodeling.</div>

Oxidative Medicine and Cellular Longevity

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Figure 7

Figure 7: Hyperglycemia Induces Endoplasmic Reticulum Stress in Atrial Cardiomyocytes, and Mitofusin-2 Downregulation Prevents Mitochondrial Dysfunction and Subsequent Cell Death 

Figure 7 | Hyperglycemia Induces Endoplasmic Reticulum Stress in Atrial Cardiomyocytes, and Mitofusin-2 Downregulation Prevents Mitochondrial Dysfunction and Subsequent Cell Death 