The Role of Ferroptosis in Adverse Left Ventricular Remodeling Following Acute Myocardial Infarction.
The Role of Ferroptosis in Adverse Left Ventricular Remodeling Following Acute Myocardial Infarction.
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DOI：
10.3390/cells11091399
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发表时间：
2022-04-20
期刊：
影响因子：
6
通讯作者：
Matsui, Takashi
中科院分区：
文献类型：
--
作者：
Komai, Kyoko;Kawasaki, Nicholas K.;Higa, Jason K.;Matsui, Takashi
铁凋亡是一种铁依赖性形式的调节性细胞死亡，与其他常规形式的调节性细胞死亡不同。它通常以抗氧化剂硒蛋白谷胱甘肽过氧化物酶4（GPX 4）抗氧化系统的功能障碍为特征。这种抗氧化能力的丧失导致脂质过氧化和随后的质膜结构受损。GPX 4抗氧化系统的破坏与各种疾病有关，如心肌病和缺血-再灌注（I/R）损伤。GPX 4调节脂质过氧化，GPX 4的化学或遗传抑制导致心脏功能降低。铁螯合剂或抗氧化剂可用于抑制铁凋亡，其在体内和离体实验中恢复功能并赋予针对I/R损伤的总体心脏保护作用。此外，抑制铁凋亡还抑制炎症反应，限制I/R损伤后左心室重构的程度。未来的研究是必要的，以了解缺血事件后铁凋亡的作用，并可能导致发现更多潜在的治疗方法，防止心脏铁凋亡。
Ferroptosis is an iron-dependent form of regulated cell death and is distinct from other conventional forms of regulated cell death. It is often characterized by the dysfunction of the antioxidant selenoprotein glutathione peroxidase 4 (GPX4) antioxidant system. This loss of antioxidant capacity leads to the peroxidation of lipids and subsequent compromised plasma membrane structure. Disruption of the GPX4 antioxidant system has been associated with various conditions such as cardiomyopathy and ischemia-reperfusion (I/R) injury. GPX4 regulates lipid peroxidation, and chemical or genetic inhibition of GPX4 leads to reduced cardiac function. Iron chelators or antioxidants can be used for inhibiting ferroptosis, which restores functionality in in vivo and ex vivo experiments and confers overall cardioprotective effects against I/R injury. Moreover, suppression of ferroptosis also suppresses inflammation and limits the extent of left ventricle remodeling after I/R injury. Future research is necessary to understand the role of ferroptosis following an ischemic incident and can lead to the discovery of more potential therapeutics that prevent ferroptosis in the heart.
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ACSL4 通过塑造细胞脂质成分来决定铁死亡敏感性。
影响因子：
14.8
作者：
Doll S;Proneth B;Tyurina YY;Panzilius E;Kobayashi S;Ingold I;Irmler M;Beckers J;Aichler M;Walch A;Prokisch H;Trümbach D;Mao G;Qu F;Bayir H;Füllekrug J;Scheel CH;Wurst W;Schick JA;Kagan VE;Angeli JP;Conrad M
通讯作者：
Conrad M
影响因子：
64.5
作者：
Dixon SJ;Lemberg KM;Lamprecht MR;Skouta R;Zaitsev EM;Gleason CE;Patel DN;Bauer AJ;Cantley AM;Yang WS;Morrison B 3rd;Stockwell BR
通讯作者：
Stockwell BR
影响因子：
21.3
作者：
Friedmann Angeli JP;Schneider M;Proneth B;Tyurina YY;Tyurin VA;Hammond VJ;Herbach N;Aichler M;Walch A;Eggenhofer E;Basavarajappa D;Rådmark O;Kobayashi S;Seibt T;Beck H;Neff F;Esposito I;Wanke R;Förster H;Yefremova O;Heinrichmeyer M;Bornkamm GW;Geissler EK;Thomas SB;Stockwell BR;O'Donnell VB;Kagan VE;Schick JA;Conrad M
通讯作者：
Conrad M
影响因子：
11.4
作者：
Fradejas-Villar N;Zhao W;Reuter U;Doengi M;Ingold I;Bohleber S;Conrad M;Schweizer U
通讯作者：
Schweizer U
心肌铁蛋白 H 缺失通过 Slc7a11 介导的铁死亡促进心肌病
影响因子：
20.1
作者：
Fang, Xuexian;Cai, Zhaoxian;Wang, Fudi
通讯作者：
Wang, Fudi