Matches in SemOpenAlex for { <https://semopenalex.org/work/W4375843430> ?p ?o ?g. }
- W4375843430 endingPage "114830" @default.
- W4375843430 startingPage "114830" @default.
- W4375843430 abstract "Recently, cuproptosis has been demonstrated to be a new non-apototic cell death mode that is characterized by copper dependence and the regulation of mitochondrial respiration. Cuproptosis is distinct from known cell death modes such as apoptosis, necrosis, pyroptosis, or ferroptosis. Excessive copper induces cuproptosis by promoting protein toxic stress reactions via copper-dependent anomalous oligomerization of lipoylation proteins in the tricarboxylic acid (TCA) cycle and reducing iron-sulfur cluster protein levels. Ferredoxin1 (FDX1) promotes dihydrolipoyl transacetylase (DLAT) lipoacylation and abates iron-sulfur cluster proteins by reducing Cu2+ to Cu+, inducing cell death. Copper homeostasis depends on the copper transporter, and disturbances to this homeostasis cause cuproptosis. Recent evidence has shown that cuproptosis plays a significant role in the occurrence and development of many cardiovascular diseases, such as myocardial ischemia/reperfusion (I/R) injury, heart failure, atherosclerosis, and arrhythmias. Copper chelators, such as ammonium tetrathiomolybdate(VI) and DL-Penicillamine, may ease the above cardiovascular diseases by inhibiting the cuproptosis pathway. Oxidative phosphorylation inhibitors may inhibit cuproptosis by inhibiting protein stress response. In conclusion, cuproptosis plays an essential role in cardiovascular disease pathogenesis. Inhibition of cardiovascular cuproptosis is expected to become a potential treatment. Here, we will thoroughly review the molecular mechanisms involved in cuproptosis and its significance in cardiovascular disease." @default.
- W4375843430 created "2023-05-10" @default.
- W4375843430 creator A5018706042 @default.
- W4375843430 creator A5021799514 @default.
- W4375843430 creator A5028705199 @default.
- W4375843430 creator A5029360035 @default.
- W4375843430 creator A5046983250 @default.
- W4375843430 creator A5052304130 @default.
- W4375843430 creator A5065669986 @default.
- W4375843430 creator A5068932388 @default.
- W4375843430 creator A5086192978 @default.
- W4375843430 date "2023-07-01" @default.
- W4375843430 modified "2023-10-14" @default.
- W4375843430 title "The molecular mechanisms of cuproptosis and its relevance to cardiovascular disease" @default.
- W4375843430 cites W1040932215 @default.
- W4375843430 cites W1515706775 @default.
- W4375843430 cites W1938192410 @default.
- W4375843430 cites W1958022600 @default.
- W4375843430 cites W1964335164 @default.
- W4375843430 cites W1966736088 @default.
- W4375843430 cites W1972494250 @default.
- W4375843430 cites W1980095667 @default.
- W4375843430 cites W1981182593 @default.
- W4375843430 cites W1989421692 @default.
- W4375843430 cites W1991633628 @default.
- W4375843430 cites W1997854913 @default.
- W4375843430 cites W2011043431 @default.
- W4375843430 cites W2015086526 @default.
- W4375843430 cites W2017238265 @default.
- W4375843430 cites W2020604453 @default.
- W4375843430 cites W2021878575 @default.
- W4375843430 cites W2027822748 @default.
- W4375843430 cites W2028162396 @default.
- W4375843430 cites W2036180531 @default.
- W4375843430 cites W2037534055 @default.
- W4375843430 cites W2045208621 @default.
- W4375843430 cites W2047653529 @default.
- W4375843430 cites W2047946880 @default.
- W4375843430 cites W2048494900 @default.
- W4375843430 cites W2050310982 @default.
- W4375843430 cites W2061460308 @default.
- W4375843430 cites W2062445592 @default.
- W4375843430 cites W2077477440 @default.
- W4375843430 cites W2079149209 @default.
- W4375843430 cites W2080969950 @default.
- W4375843430 cites W2086464243 @default.
- W4375843430 cites W2095347327 @default.
- W4375843430 cites W2100625171 @default.
- W4375843430 cites W2109064014 @default.
- W4375843430 cites W2111208413 @default.
- W4375843430 cites W2111357564 @default.
- W4375843430 cites W2113783642 @default.
- W4375843430 cites W2115967860 @default.
- W4375843430 cites W2118295902 @default.
- W4375843430 cites W2119154675 @default.
- W4375843430 cites W2130452502 @default.
- W4375843430 cites W2145635335 @default.
- W4375843430 cites W2147653980 @default.
- W4375843430 cites W2149499310 @default.
- W4375843430 cites W2169817950 @default.
- W4375843430 cites W2320912947 @default.
- W4375843430 cites W2325016416 @default.
- W4375843430 cites W2419249444 @default.
- W4375843430 cites W2520818180 @default.
- W4375843430 cites W2607393345 @default.
- W4375843430 cites W2754663667 @default.
- W4375843430 cites W2772508026 @default.
- W4375843430 cites W2791721322 @default.
- W4375843430 cites W2801173089 @default.
- W4375843430 cites W2806100248 @default.
- W4375843430 cites W2883785633 @default.
- W4375843430 cites W2908546557 @default.
- W4375843430 cites W2915844415 @default.
- W4375843430 cites W2942814044 @default.
- W4375843430 cites W2945294912 @default.
- W4375843430 cites W2981918029 @default.
- W4375843430 cites W3003463158 @default.
- W4375843430 cites W3012085768 @default.
- W4375843430 cites W3017313996 @default.
- W4375843430 cites W3088729674 @default.
- W4375843430 cites W3093379091 @default.
- W4375843430 cites W3119659742 @default.
- W4375843430 cites W3129908464 @default.
- W4375843430 cites W3149519194 @default.
- W4375843430 cites W3180244450 @default.
- W4375843430 cites W3203371090 @default.
- W4375843430 cites W3203838768 @default.
- W4375843430 cites W4210757594 @default.
- W4375843430 cites W4214820008 @default.
- W4375843430 cites W4220757518 @default.
- W4375843430 cites W4221016006 @default.
- W4375843430 cites W4221115671 @default.
- W4375843430 cites W4242459468 @default.
- W4375843430 cites W4280497443 @default.
- W4375843430 cites W4280582251 @default.
- W4375843430 cites W4281717038 @default.
- W4375843430 cites W4286493081 @default.
- W4375843430 cites W4293083602 @default.