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  • Magtanong et al observed that caspase dependent

    2021-10-23

    Magtanong et al. (2019) observed that caspase-dependent apoptotic lipotoxicity of saturated fatty acids is suppressed by exogenous MUFAs. This may explain the ability of MUFAs to prevent atherosclerosis, in contrast to the pathogenicity of saturated fatty acids. Moreover, MUFAs may promote while PUFAs suppress cancer cell growth by enhancing peroxidation process to induce ferroptosis/apoptosis. Thus, MUFAs and PUFAs need to be carefully orchestrated to prevent atherosclerosis and cancer. It is noteworthy that lymphokine activated macrophages bring about their tumoricidal action by releasing PUFAs (gamma-linolenic acid/alpha-linolenic acid) (Schlager et al., 1983). TNF-α inhibits the activity of desaturases and thus induces an AA-deficient state (Mayer et al., 2002) and consequently LXA4 production will be decreased but PGE2 levels will be high., whereas AA and PGE2 suppress TNF-α formation. This close interaction between MUFA and PUFA metabolism, cytokines, ROS, GPX4/vitamin E, and ferroptosis may ultimately determine tumor cell survival or ferroptosis. Thus, methods designed to deliver PUFAs direct and/or enhance ROS and lipid peroxidation process selectively in tumor diltiazem hcl may be a potentially powerful approach to cancer treatment.
    Introduction Various types of cell death such as apoptosis, ferroptosis and autophagic cell death play an important role in myocardial homeostasis and pathology [1,2]. Ferroptosis is a recently identified type of regulated cell death characterized by the iron-dependent accumulation of lipid ROS [3]. It is regulated by multiple signal pathways such as α6β4 integrin and NRF2-Keap1 axis [4,5]. Many regulators such as glutathione peroxidase 4 (GPX4), NRF2, p53, heme oxygenase-1 and acyl-CoA synthetase long-chain family member 4 (ACSL4) have been identified to be involved in regulation of cell ferroptosis [[6], [7], [8]]. Ferroptosis has been implicated in the pathology of a variety of diseases such as tumors, tissue or organ injury, stroke, ischemia-reperfusion injury and kidney degeneration [9,10]. However, its biological roles and regulation pathways in heart diseases remain poorly understood. New insight into observation of cardiomyocytes ferroptosis may provide new diagnostic and therapeutic approaches for cardiovascular diseases. Bioactive lipids such as lysophosphatidic acid (LPA) and sphingosine-phosphate (S1P) play important roles in both physiological and pathophysiological processes including angiogenesis, inflammation, fibrosis and carcinogenesis [[11], [12], [13]]. LPA, a bioactive phospholipids with diverse functions, acts as an autocrine/paracrine messenger by activation of its G protein-coupled receptors [14]. Autotaxin (ATX), also termed ENPP2, is a secreted enzyme important for generating LPA [15]. Disturbances in normal ATX-LPA signaling is associated to a range of diseases including cardiovascular disease. Cardiomyocytes express LPA receptor subtypes including LPA1-LPA5. These receptors mediate LPA-induced hypertrophy of neonatal cardiac myocytes via activation of Gi and Rho [16]. LPA also mediated augmentation of cardiomyocytes lipoprotein lipase and involved in both acute and chronic ischemic cardiac damage [17,18]. However, the regulatory roles of ATX-LPA signaling in regulating of cardiomyocytes characteristics have less been explored. In this study, we investigated the regulatory roles of ATX-LPA signaling in erastin-induced ferroptosis of cardiomyocytes and elucidate its mechanisms.
    Materials and methods
    Results
    Discussion ENPP2/LPA signaling is involved in regulating various types of regulated cell death such as apoptosis, necroptosis and autophagy [19,20]. Ferroptosis was recently reported as a novel mechanism of iron-dependent regulated cell death. Its roles in myocardial homeostasis and pathology of heart diseases are not well understood. In this study, we demonstrated that ENPP2/LPA inhibits erastin-induced ferroptosis in cardiomyocytes and may play a novel role in myocardial homeostasis.