[1]
|
Boyle A J,Shih H,Hwang J,et al. Cardiomyopathy of aging in the mammalian heart is characterized by myocardial hypertrophy,fibrosis and a predisposition towards cardiomyocyte apoptosis and autophagy[J]. Experimental Gerontology,2011,46(7):549-559. doi: 10.1016/j.exger.2011.02.010
|
[2]
|
Elliott P,Andersson B,Arbustini E,et al. Classification of the cardiomyopathies: A position statement from the european society of cardiology working group on myocardial and pericardial diseases[J]. European Heart Journal,2007,29(2):270-276. doi: 10.1093/eurheartj/ehm342
|
[3]
|
Djulbegovic M B,Uversky V N. Ferroptosis – An iron- and disorder-dependent programmed cell death[J]. International Journal of Biological Macromolecules,2019,135:1052-1069. doi: 10.1016/j.ijbiomac.2019.05.221
|
[4]
|
Kapralov A A,Yang Q,Dar H H,et al. Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death.[J]. Nature Chemical Biology,2020,16(3):278-290. doi: 10.1038/s41589-019-0462-8
|
[5]
|
Jiang X,Stockwell B R,Conrad M. Ferroptosis: Mechanisms,biology,and role in disease[J]. Nature Reviews. Molecular Cell Biology,2021,22(4):266-282. doi: 10.1038/s41580-020-00324-8
|
[6]
|
Bannai S,Kitamura E. Transport interaction of L-cystine and L-glutamate in human diploid fibroblasts in culture.[J]. Biological Chemistry,1980,255(6):2372-2376. doi: 10.1016/S0021-9258(19)85901-X
|
[7]
|
Yang W S,Stockwell B R. Synthetic lethal screening identifies compounds activating iron-dependent,nonapoptotic cell death in oncogenic-RAS-harboring cancer cells[J]. Chemistry & Biology,2008,15(3):234-245.
|
[8]
|
Dixon S J,Lemberg K M,Lamprecht M R,et al. Ferroptosis: an iron-dependent form of non-apoptotic cell death[J]. Cell,2012,149(5):1060-1072. doi: 10.1016/j.cell.2012.03.042
|
[9]
|
Anderson G J,Vulpe C D. Mammalian iron transport[J]. Cellular and Molecular Life Sciences,2009,66(20):3241-3261. doi: 10.1007/s00018-009-0051-1
|
[10]
|
Torti S V,Torti F M. Iron and cancer: 2020 vision[J]. Cancer Research,2020,80(24):5435-5448. doi: 10.1158/0008-5472.CAN-20-2017
|
[11]
|
Dixon S J,Stockwell B R. The role of iron and reactive oxygen species in cell death[J]. Nature Chemical Biology,2014,10(1):9-17. doi: 10.1038/nchembio.1416
|
[12]
|
Gao M,Monian P,Pan Q,et al. Ferroptosis is an autophagic cell death process[J]. Cell Research,2016,26(9):1021-1032. doi: 10.1038/cr.2016.95
|
[13]
|
Bridges R J,Natale N R,Patel S A. System xc-cystine/glutamate antiporter: an update on molecular pharmacology and roles within the CNS[J]. British Journal of Pharmacology,2012,165(1):20-34. doi: 10.1111/j.1476-5381.2011.01480.x
|
[14]
|
Shah R,Margison K,Pratt D A. The potency of diarylamine radical-trapping antioxidants as inhibitors of ferroptosis underscores the role of autoxidation in the mechanism of cell death[J]. ACS Chemical Biology,2017,12(10):2538-2545. doi: 10.1021/acschembio.7b00730
|
[15]
|
Had-Aissouni L. Maintenance of antioxidant defenses of brain cells: plasma membrane glutamate transporters and beyond[J]. Amino Acids,2012,42(1):159-161. doi: 10.1007/s00726-011-0860-z
|
[16]
|
Yang W S,SriRamaratnam R,Welsch M E,et al. Regulation of ferroptotic cancer cell death by GPX4[J]. Cell,2014,156(1-2):317-331.
|
[17]
|
Yang W S,Stockwell B R. Ferroptosis: death by lipid peroxidation[J]. Trends in Cell Biology,2016,26(3):165-176. doi: 10.1016/j.tcb.2015.10.014
|
[18]
|
Shimada K,Skouta R,Kaplan A,et al. Global survey of cell death mechanisms reveals metabolic regulation of ferroptosis[J]. Nature Chemical Biology,2016,12(7):497-503. doi: 10.1038/nchembio.2079
|
[19]
|
Hassannia B,Vandenabeele P,Vanden Berghe T. Targeting ferroptosis to iron out cancer[J]. Cancer Cell,2019,35(6):830-849. doi: 10.1016/j.ccell.2019.04.002
|
[20]
|
Yang W S,Kim K J,Gaschler M M,et al. Peroxidation of polyunsaturated fatty acids by lipoxygenases drives ferroptosis[J]. Proceedings of the National Academy of Sciences of the United States of America,2016,113(34):E4966-E4975.
|
[21]
|
Kagan V E,Mao G,Qu F,et al. Oxidized arachidonic/adrenic phosphatidylethanolamines navigate cells to ferroptosis[J]. Nature Chemical Biology,2017,13(1):81-90. doi: 10.1038/nchembio.2238
|
[22]
|
Dixon S J,Winter G E,Musavi L S,et al. Human haploid cell genetics reveals roles for lipid metabolism genes in nonapoptotic cell death[J]. ACS Chemical Biology,2015,10(7):1604-1609. doi: 10.1021/acschembio.5b00245
|
[23]
|
Golej D L,Askari B,Kramer F,et al. Long-chain acyl-CoA synthetase 4 modulates prostaglandin E2 release from human arterial smooth muscle cells[J]. Journal of Lipid Research,2011,52(4):782-793. doi: 10.1194/jlr.M013292
|
[24]
|
Tadokoro T, Ikeda M, Ide T, et al. Mitochondria-dependent ferroptosis plays a pivotal role in doxorubicin cardiotoxicity[J]. JCI Insight, 2020, 5(9): e132747.
|
[25]
|
Bersuker K,Hendricks J,Li Z,et al. The CoQ oxidoreductase FSP1 acts in parallel to GPX4 to inhibit ferroptosis[J]. Nature,2019,575(7784):688-692. doi: 10.1038/s41586-019-1705-2
|
[26]
|
Dai E,Zhang W,Cong D,et al. AIFM2 blocks ferroptosis independent of ubiquinol metabolism[J]. Biochemical and Biophysical Research Communications,2020,523(4):966-971. doi: 10.1016/j.bbrc.2020.01.066
|
[27]
|
McGowan J V,Chung R,Maulik A,et al. Anthracycline chemotherapy and cardiotoxicity[J]. Cardiovascular Drugs and Therapy,2017,31(1):63-75. doi: 10.1007/s10557-016-6711-0
|
[28]
|
Wang G,Hamid T,Keith R J,et al. Cardioprotective and anti-apoptotic effects of heme oxygenase-1in the failing heart[J]. Circulation,2010,121(17):1912-1925. doi: 10.1161/CIRCULATIONAHA.109.905471
|
[29]
|
Liu Y,Zeng L,Yang Y,et al. Acyl-CoA thioesterase 1 prevents cardiomyocytes from doxorubicin-induced ferroptosis via shaping the lipid composition[J]. Cell Death & Disease,2020,11(9):756.
|
[30]
|
Rhee J W,Yi H,Thomas D,et al. Modeling secondary iron overload cardiomyopathy with human induced pluripotent stem cell-derived cardiomyocytes[J]. Cell Reports,2020,32(2):107886. doi: 10.1016/j.celrep.2020.107886
|
[31]
|
DeHart D N,Fang D,Heslop K,et al. Opening of voltage dependent anion channels promotes reactive oxygen species generation,mitochondrial dysfunction and cell death in cancer cells[J]. Biochemical Pharmacology,2018,148(1):155-162. doi: 10.1016/j.bcp.2017.12.022
|
[32]
|
Wang C,Yuan W,Hu A,et al. Dexmedetomidine alleviated sepsis-induced myocardial ferroptosis and septic heart injury[J]. Molecular Medicine Reports,2020,22(1):175-184. doi: 10.3892/mmr.2020.11114
|
[33]
|
A Thandavarayan R,V Giridharan V,Watanabe K,et al. Diabetic cardiomyopathy and oxidative stress: Role of antioxidants[J]. Cardiovascular & Hematological Agents in Medicinal Chemistry,2011,9(4):225-230.
|
[34]
|
Zang H,Wu W,Qi L,et al. Autophagy inhibition enables nrf2 to exaggerate the progression of diabetic cardiomyopathy in mice[J]. Diabetes,2020,69(12):2720-2734. doi: 10.2337/db19-1176
|
[35]
|
Schultheis J, Beckmann D, Mulac D, et al. Nrf2 activation protects mouse beta cells from glucolipotoxicity by restoring mitochondrial function and physiological redox balance[J]. Oxidative Medicine and Cellular Longevity, 2019, 2019: 7518510.
|
[36]
|
Bao L,Jin Y,Han J,et al. Berberine regulates GPX4 to inhibit ferroptosis of islet β cells[J]. Planta Medica,2023,89(3):254-261. doi: 10.1055/a-1939-7417
|
[37]
|
Mei S,Xia Z,Qiu Z,et al. Shenmai injection attenuates myocardial ischemia/reperfusion injury by targeting Nrf2/GPX4 signalling-mediated ferroptosis[J]. Chinese Journal of Integrative Medicine,2022,28(11):983-991. doi: 10.1007/s11655-022-3620-x
|
[38]
|
Li K. Iron pathophysiology in friedreich's ataxia[J]. Advances in Experimental Medicine and Biology,2019,1173(1):125-143.
|
[39]
|
Zhang S,Napierala M,Napierala J S. Therapeutic prospects for Friedreich’s ataxia[J]. Trends in Pharmacological Sciences,2019,40(4):229-233. doi: 10.1016/j.tips.2019.02.001
|
[40]
|
Emond M,Lepage G,Vanasse M,et al. Increased levels of plasma malondialdehyde in Friedreich ataxia[J]. Neurology,2000,55(11):1752-1753. doi: 10.1212/WNL.55.11.1752
|
[41]
|
Kahn-Kirby A H,Amagata A,Maeder C I,et al. Targeting ferroptosis: A novel therapeutic strategy for the treatment of mitochondrial disease-related epilepsy[J]. PLoS ONE,2019,14(3):e0214250. doi: 10.1371/journal.pone.0214250
|