Cardioprotection Attributed to Aerobic Exercise-Mediated Inhibition of ALCAT1 and Oxidative Stress-Induced Apoptosis in MI Rats

Abstract

Cardiolipin (CL) plays a pivotal role in mitochondria-mediated apoptosis. Acyl-CoA: lysocardiolipin acyltransferase 1 (ALCAT1) can accelerate CL reactive oxygen production and cause mitochondrial damage. Although we have demonstrated that aerobic exercise significantly reduced ALCAT1 levels in MI mice, what is the temporal characteristic of ALCAT1 after MI? Little is known. Based on this, the effect of exercise on ALCAT1 in MI rats needs to be further verified. Therefore, this paper aimed to characterize ALCAT1 expression, and investigate the possible impact of exercise on ALCAT1 and its role in fibrosis, antioxidant capacity, and apoptosis in MI rats. Our results indicated that the potential utility of MI increased ALCAT1 expression within 1–6 h of MI, and serum CK and CKMB had significant effects in MI at 24 h, while LDH exerted an effect five days after MI. Furthermore, ALCAT1 expression was upregulated, oxidative capacity and excessive apoptosis were enhanced, and cardiac function was decreased after MI, and aerobic exercise can reverse these changes. These findings revealed a previously unknown endogenous cardiac injury factor, ALCAT1, and demonstrated that ALCAT1 damaged the heart of MI rats, and aerobic exercise reduced ALCAT1 expression, oxidative stress, and apoptosis after MI-induced cardiac injury in rats.

Effect of miR-182-5p on apoptosis in myocardial infarction

“…Numerous studies connect ischemic cardiomyopathy and specific congenital heart diseases to cell apoptosis [ 17 , 20 , 21 ]. The consequences of ischemia- and hypoxia-induced myocardial cell apoptosis are severe, leading to adverse cardiac outcomes such as ventricular remodeling [ 11 , 22 , 23 ].…”

Molecular Mechanisms and Mediators of Hepatotoxicity Resulting from an Excess of Lipids and Non-Alcoholic Fatty Liver Disease

“…Observations from a few studies using obese mice with leptin deficiency (ob/ob) and leptin receptor deficiency (db/db), as well as many in vitro lipotoxicity models, suggest that the hepatotoxic effects of FFAs are not mediated by RIPK1-dependent signal pathways, but rather by mitochondrial apoptosis and death-receptor-transduced signals [93,94]. In particular, TRAIL receptor overexpression [95]; ROS production [96]; BAX binding with p-MLKL mediating lysosomal membrane permeabilization [97]; activation of the tumor suppressor protein p53 [98]; and direct mitochondriotoxic effects induced by the local accumulation of modified lipids, such as oxidized cardiolipin [99] and ceramides [100], appear to be involved in FFA-induced apoptosis. It has been shown, in support of this hypothesis, that a combination of saturated fatty acids, such as palmitic and oleic acid, increases the sensibility of hepatocytes to the induction of cell death by a variety of stimuli [101,102].…”

Aerobic exercise protects MI heart through miR-133a-3p downregulation of connective tissue growth factor

“…Myocardial ischemia and hypoxia after myocardial infarction (MI) lead to oxidative stress, apoptosis, ventricular malignant remodeling, inflammatory response and deterioration of cardiac function, eventually developing into heart failure [1][2][3]. Physical exercise is one of the most important tools for cardiovascular disease prevention and rehabilitation [4], and appropriate exercise can inhibit myocardial apoptosis [5,6], improve myocardial pathological remodeling [7], promote revascularization [8], reduce myocardial fibrosis [9], and improve left ventricular systolic dysfunction [10]. Aerobic exercise can maximize the cardioprotective effects of exercise [10], but its targets and mechanisms of action have not been elucidated.…”