Matches in SemOpenAlex for { <https://semopenalex.org/work/W4294152357> ?p ?o ?g. }
- W4294152357 endingPage "2726" @default.
- W4294152357 startingPage "2726" @default.
- W4294152357 abstract "Ferroptosis has recently been demonstrated to be a novel regulated non-apoptotic cell death characterized by iron-dependence and the accumulation of lipid peroxidation that results in membrane damage. Excessive iron induces ferroptosis by promoting the generation of both soluble and lipid ROS via an iron-dependent Fenton reaction and lipoxygenase (LOX) enzyme activity. Cytosolic glutathione peroxidase 4 (cGPX4) pairing with ferroptosis suppressor protein 1 (FSP1) and mitochondrial glutathione peroxidase 4 (mGPX4) pairing with dihydroorotate dehydrogenase (DHODH) serve as two separate defense systems to detoxify lipid peroxidation in the cytoplasmic as well as the mitochondrial membrane, thereby defending against ferroptosis in cells under normal conditions. However, disruption of these defense systems may cause ferroptosis. Emerging evidence has revealed that ferroptosis plays an essential role in the development of diverse cardiovascular diseases (CVDs), such as hemochromatosis-associated cardiomyopathy, doxorubicin-induced cardiotoxicity, ischemia/reperfusion (I/R) injury, heart failure (HF), atherosclerosis, and COVID-19–related arrhythmias. Iron chelators, antioxidants, ferroptosis inhibitors, and genetic manipulations may alleviate the aforementioned CVDs by blocking ferroptosis pathways. In conclusion, ferroptosis plays a critical role in the pathogenesis of various CVDs and suppression of cardiac ferroptosis is expected to become a potential therapeutic option. Here, we provide a comprehensive review on the molecular mechanisms involved in ferroptosis and its implications in cardiovascular disease." @default.
- W4294152357 created "2022-09-02" @default.
- W4294152357 creator A5018736245 @default.
- W4294152357 creator A5035066579 @default.
- W4294152357 creator A5055464992 @default.
- W4294152357 creator A5084773942 @default.
- W4294152357 date "2022-09-01" @default.
- W4294152357 modified "2023-10-18" @default.
- W4294152357 title "Molecular Mechanisms of Ferroptosis and Relevance to Cardiovascular Disease" @default.
- W4294152357 cites W1486228890 @default.
- W4294152357 cites W1523821352 @default.
- W4294152357 cites W1527438616 @default.
- W4294152357 cites W1928298896 @default.
- W4294152357 cites W1974922478 @default.
- W4294152357 cites W1981982065 @default.
- W4294152357 cites W1990350441 @default.
- W4294152357 cites W1997183854 @default.
- W4294152357 cites W2001084458 @default.
- W4294152357 cites W2002490399 @default.
- W4294152357 cites W2006536535 @default.
- W4294152357 cites W2007761806 @default.
- W4294152357 cites W2008295373 @default.
- W4294152357 cites W2008757142 @default.
- W4294152357 cites W2011052121 @default.
- W4294152357 cites W2016751278 @default.
- W4294152357 cites W2024287748 @default.
- W4294152357 cites W2035898183 @default.
- W4294152357 cites W2040564306 @default.
- W4294152357 cites W2043614277 @default.
- W4294152357 cites W2052980342 @default.
- W4294152357 cites W2057632732 @default.
- W4294152357 cites W2058581405 @default.
- W4294152357 cites W2060035882 @default.
- W4294152357 cites W2062742764 @default.
- W4294152357 cites W2065377708 @default.
- W4294152357 cites W2067107606 @default.
- W4294152357 cites W2067490363 @default.
- W4294152357 cites W2070943914 @default.
- W4294152357 cites W2076768785 @default.
- W4294152357 cites W2081053802 @default.
- W4294152357 cites W2083867296 @default.
- W4294152357 cites W2084304742 @default.
- W4294152357 cites W2087952741 @default.
- W4294152357 cites W2091926090 @default.
- W4294152357 cites W2093061584 @default.
- W4294152357 cites W2112885253 @default.
- W4294152357 cites W2114138419 @default.
- W4294152357 cites W2122341467 @default.
- W4294152357 cites W2126751267 @default.
- W4294152357 cites W2140182328 @default.
- W4294152357 cites W2163005196 @default.
- W4294152357 cites W2231291760 @default.
- W4294152357 cites W2265062179 @default.
- W4294152357 cites W2275746735 @default.
- W4294152357 cites W2284262522 @default.
- W4294152357 cites W2508296626 @default.
- W4294152357 cites W2513656923 @default.
- W4294152357 cites W2515712940 @default.
- W4294152357 cites W2549188196 @default.
- W4294152357 cites W2550324626 @default.
- W4294152357 cites W2566407837 @default.
- W4294152357 cites W2592029987 @default.
- W4294152357 cites W2592384159 @default.
- W4294152357 cites W2621833341 @default.
- W4294152357 cites W2749918768 @default.
- W4294152357 cites W2762087180 @default.
- W4294152357 cites W2767127256 @default.
- W4294152357 cites W2767876404 @default.
- W4294152357 cites W2788640168 @default.
- W4294152357 cites W2792682639 @default.
- W4294152357 cites W2793937397 @default.
- W4294152357 cites W2794703348 @default.
- W4294152357 cites W2795028304 @default.
- W4294152357 cites W2799476686 @default.
- W4294152357 cites W2803347838 @default.
- W4294152357 cites W2805186935 @default.
- W4294152357 cites W2807667881 @default.
- W4294152357 cites W2885025259 @default.
- W4294152357 cites W2887801652 @default.
- W4294152357 cites W2890597423 @default.
- W4294152357 cites W2896506245 @default.
- W4294152357 cites W2898371604 @default.
- W4294152357 cites W2904639698 @default.
- W4294152357 cites W2906319220 @default.
- W4294152357 cites W2909817598 @default.
- W4294152357 cites W2911295209 @default.
- W4294152357 cites W2913973491 @default.
- W4294152357 cites W2914574872 @default.
- W4294152357 cites W2916144846 @default.
- W4294152357 cites W2924471609 @default.
- W4294152357 cites W2935369648 @default.
- W4294152357 cites W2950662228 @default.
- W4294152357 cites W2964465172 @default.
- W4294152357 cites W2968121100 @default.
- W4294152357 cites W2979799294 @default.
- W4294152357 cites W2980472864 @default.
- W4294152357 cites W2981179816 @default.
- W4294152357 cites W2990511618 @default.