Ferroptosis and Senescence: A Systematic Review

被引:42
作者
Coradduzza, Donatella [1 ]
Congiargiu, Antonella [1 ]
Chen, Zhichao [1 ]
Zinellu, Angelo [1 ]
Carru, Ciriaco [1 ,2 ]
Medici, Serenella [3 ]
机构
[1] Univ Sassari, Dept Biomed Sci, I-07100 Sassari, Italy
[2] Azienda Ospedaliera Univ AOU, Control Qual Unit, I-07100 Sassari, Italy
[3] Univ Sassari, Dept Chem Phys Math & Nat Sci, I-07100 Sassari, Italy
关键词
ferroptosis; senescence; aging; disease; IRON ACCUMULATION; CANCER-THERAPY; MECHANISMS; NECROPTOSIS; HOMEOSTASIS; METABOLISM; REGULATOR; BIOLOGY;
D O I
10.3390/ijms24043658
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Senescence is a cellular aging process in all multicellular organisms. It is characterized by a decay in cellular functions and proliferation, resulting in increased cellular damage and death. This condition plays an essential role in the aging process and significantly contributes to the development of age-related complications. On the other hand, ferroptosis is a systemic cell death pathway characterized by excessive iron accumulation followed by the generation of reactive oxygen species (ROS). Oxidative stress is a common trigger of this condition and may be induced by various factors such as toxins, drugs, and inflammation. Ferroptosis is linked to numerous disorders, including cardiovascular disease, neurodegeneration, and cancer. Senescence is believed to contribute to the decay in tissue and organ functions occurring with aging. It has also been linked to the development of age-related pathologies, such as cardiovascular diseases, diabetes, and cancer. In particular, senescent cells have been shown to produce inflammatory cytokines and other pro-inflammatory molecules that can contribute to these conditions. In turn, ferroptosis has been linked to the development of various health disorders, including neurodegeneration, cardiovascular disease, and cancer. Ferroptosis is known to play a role in the development of these pathologies by promoting the death of damaged or diseased cells and contributing to the inflammation often associated. Both senescence and ferroptosis are complex pathways that are still not fully understood. Further research is needed to thoroughly investigate the role of these processes in aging and disease, and to identify potential interventions to target such processes in order to prevent or treat age-related conditions. This systematic review aims to assess the potential mechanisms underlying the link connecting senescence, ferroptosis, aging, and disease, and whether they can be exploited to block or limit the decay of the physiological functions in elderly people for a healthy longevity.
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页数:15
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共 70 条
[31]   Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis [J].
Masaldan, Shashank ;
Clatworthy, Sharnel A. S. ;
Gamell, Cristina ;
Meggyesy, Peter M. ;
Rigopoulos, Antonia-Tonia ;
Haupt, Sue ;
Haupt, Ygal ;
Denoyer, Delphine ;
Adlard, Paul A. ;
Bush, Ashley I. ;
Cater, Michael A. .
REDOX BIOLOGY, 2018, 14 :100-115
[32]   Sites of erythropoietin production [J].
Maxwell, PH ;
Ferguson, DJP ;
Nicholls, LG ;
Iredale, JP ;
Pugh, CW ;
Johnson, MH ;
Ratcliffe, PJ .
KIDNEY INTERNATIONAL, 1997, 51 (02) :393-401
[33]   Implication of ferroptosis in aging [J].
Mazhar, Maryam ;
Din, Ahmad Ud ;
Ali, Hamid ;
Yang, Guoqiang ;
Ren, Wei ;
Wang, Li ;
Fan, Xiaohui ;
Yang, Sijin .
CELL DEATH DISCOVERY, 2021, 7 (01)
[34]   RPE65 is the isomerohydrolase in the retinoid visual cycle [J].
Moiseyev, G ;
Chen, Y ;
Takahashi, Y ;
Wu, BX ;
Ma, JX .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (35) :12413-12418
[35]   Could Conservative Iron Chelation Lead to Neuroprotection in Amyotrophic Lateral Sclerosis? [J].
Moreau, Caroline ;
Danel, Veronique ;
Devedjian, Jean Christophe ;
Grolez, Guillaume ;
Timmerman, Kelly ;
Laloux, Charlotte ;
Petrault, Maud ;
Gouel, Flore ;
Jonneaux, Aurelie ;
Dutheil, Mary ;
Lachaud, Cedrick ;
Lopes, Renaud ;
Kuchcinski, Gregory ;
Auger, Florent ;
Kyheng, Maeva ;
Duhamel, Alain ;
Perez, Thierry ;
Pradat, Pierre Francois ;
Blasco, Helene ;
Veyrat-Durebex, Charlotte ;
Corcia, Philippe ;
Oeckl, Patrick ;
Otto, Markus ;
Dupuis, Luc ;
Garcon, Guillaume ;
Defebvre, Luc ;
Cabantchik, Z. Ioav ;
Duce, James ;
Bordet, Regis ;
Devos, David .
ANTIOXIDANTS & REDOX SIGNALING, 2018, 29 (08) :742-748
[36]   Ferroptosis, a new form of cell death: opportunities and challenges in cancer [J].
Mou, Yanhua ;
Wang, Jun ;
Wu, Jinchun ;
He, Dan ;
Zhang, Chunfang ;
Duan, Chaojun ;
Li, Bin .
JOURNAL OF HEMATOLOGY & ONCOLOGY, 2019, 12
[37]   Activation of SAT1 engages polyamine metabolism with p53-mediated ferroptotic responses [J].
Ou, Yang ;
Wang, Shang-Jui ;
Li, Dawei ;
Chu, Bo ;
Gu, Wei .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2016, 113 (44) :E6806-E6812
[38]   Targeting senescent cells in translational medicine [J].
Paez-Ribes, Marta ;
Gonzalez-Gualda, Estela ;
Doherty, Gary J. ;
Munoz-Espin, Daniel .
EMBO MOLECULAR MEDICINE, 2019, 11 (12)
[39]   Targeting Ferroptosis as a Promising Therapeutic Strategy for Ischemia-Reperfusion Injury [J].
Pan, Yihang ;
Wang, Xueke ;
Liu, Xiwang ;
Shen, Lihua ;
Chen, Qixing ;
Shu, Qiang .
ANTIOXIDANTS, 2022, 11 (11)
[40]   The Chemical Biology of Ferroptosis in the Central Nervous System [J].
Ratan, Rajiv R. .
CELL CHEMICAL BIOLOGY, 2020, 27 (05) :479-498