Research Paper Volume 13, Issue 6 pp 7828—7845

Chronic metformin treatment decreases cardiac injury during ischemia-reperfusion by attenuating endoplasmic reticulum stress with improved mitochondrial function

The chronic administration of metformin decreases endoplasmic reticulum stress with improvement in cardiac mitochondrial function in aged mouse hearts. Aging increases endoplasmic reticulum (ER) stress that causes mitochondrial dysfunction by increasing calcium overload and ROS generation. The ER and cardiac mitochondrial interact via mitochondrial associated membranes (MAM). An increase in mitochondrial calcium overload and ROS generation sensitizes to mitochondrial permeability transition pore (MPTP) opening that augments cardiac injury during ischemia-reperfusion. Metformin treatment decreases cardiac injury by restoring mitochondrial function before ischemia through attenuation of the ER stress in the aged hearts.

Figure 5. The chronic administration of metformin decreases endoplasmic reticulum stress with improvement in cardiac mitochondrial function in aged mouse hearts. Aging increases endoplasmic reticulum (ER) stress that causes mitochondrial dysfunction by increasing calcium overload and ROS generation. The ER and cardiac mitochondrial interact via mitochondrial associated membranes (MAM). An increase in mitochondrial calcium overload and ROS generation sensitizes to mitochondrial permeability transition pore (MPTP) opening that augments cardiac injury during ischemia-reperfusion. Metformin treatment decreases cardiac injury by restoring mitochondrial function before ischemia through attenuation of the ER stress in the aged hearts.