Role of apoptosis in cardiovascular disease

Abstract

Apoptosis plays a key role in the pathogenesis in a variety of cardiovascular diseases due to loss of terminally differentiated cardiac myocytes. Cardiac myocytes undergoing apoptosis have been identified in tissue samples from patients suffering from myocardial infarction, diabetic cardiomyopathy, and end-stage congestive heart failure. Apoptosis is a highly regulated program of cell death and can be mediated by death receptors in the plasma membrane, as well as the mitochondria and the endoplasmic reticulum. The cell death program is activated in cardiac myocytes by various stressors including cytokines, increased oxidative stress and DNA damage. Many studies have demonstrated that inhibition of apoptosis is cardioprotective and can prevent the development of heart failure. This review provides a current overview of the evidence of apoptosis in cardiovascular diseases and discusses the molecular pathways involved in cardiac myocyte apoptosis.

Bnip3-mediated mitochondrial autophagy is independent of the mitochondrial permeability transition pore

“…In cardiac myocytes, mitochondria constitute about 30% of cell volume to ensure efficient ATP supply for the contracting myocyte. 18 As shown by staining for Cytochrome c Oxidase subunit IV (COX IV), mitochondria were very abundant in control infected myocytes (Fig. 2C).…”

Protective mechanisms of hypaconitine and glycyrrhetinic acid compatibility in oxygen and glucose deprivation injury

“…It has been proved that the PI3K/Akt signaling pathway was critical in ischemic defense and pharmacologic preconditioning of cardioprotection (Qiao et al, 2016). In order to be cardioprotective and prevent the development of heart failure, the damage of myocardial cells could be lowered via inhibiting the apoptosis process (Lee and Gustafsson, 2009). Studies also revealed that part of the mechanisms of protecting cardiomyocytes relied on the activity of Akt, which can activate the downstream spot targets, improve energy generation of mitochondria, and then decrease the pro-apoptotic factors (Tong et al, 2000).…”

Retracted: Activation of Akt Rescues Endoplasmic Reticulum Stress-Impaired Murine Cardiac Contractile Function via Glycogen Synthase Kinase-3β-Mediated Suppression of Mitochondrial Permeation Pore Opening

“…To better elucidate the interplay between ER stress and oxidative stress in ER stress-induced cardiac responses, ROS production, protein damage, apoptosis, mitochondrial integrity including mitochondrial membrane potential and mitochondrial permeation pore (mPTP) opening, as well as cell signaling of Akt and GSK3b were scrutinized in wild-type (WT) and transgenic mice with intrinsic Akt activation after ER stress induction. Levels of caspase-8 and pro-caspase-9 were assessed to evaluate the role of receptor and mitochondrial death domains, respectively (15). In addition, expression of caspase-12, an ER-specific member of the caspase family to mediate ERspecific apoptosis (28), was also monitored under ER stress and chronic Akt activation.…”