Self-defense of macrophages against oxidative injury: Fighting for their own survival

被引:82
作者
Virag, Laszlo [1 ,2 ]
Jaen, Rafael I. [3 ]
Regdon, Zsolt [1 ]
Bosca, Lisardo [3 ,4 ]
Prieto, Patricia [3 ,4 ]
机构
[1] Univ Debrecen, Dept Med Chem, Fac Med, Debrecen, Hungary
[2] MTA DE Cell Biol & Signaling Res Grp, Debrecen, Hungary
[3] UAM, CSIC, Inst Invest Biomed Alberto Sols, Arturo Duperier 4, Madrid 28029, Spain
[4] ISCIII, Ctr Invest Biomed Red Enfermedades Cardiovasc CIB, Madrid, Spain
关键词
Inflammation; Immunity; Macrophage; Oxidative burst; Metabolism; Apoptosis; Parthanatos; PARP1; NRF2; HO-1; FOXO; Antioxidant; Eicosanoids; Specialized pro-resolving mediators; Senescence; Aging; OXYGEN SPECIES GENERATION; OXIDE-DEPENDENT APOPTOSIS; TRANSCRIPTION FACTOR NRF2; NITRIC-OXIDE; LIPOXIN A(4); ALTERNATIVE ACTIVATION; KETONE-BODIES; RESOLVIN D1; FATTY-ACIDS; STRESS;
D O I
10.1016/j.redox.2019.101261
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
Activated macrophages play a central role in both the development and resolution of inflammation. These immune cells need to be functional in harmful conditions with high levels of reactive oxygen and nitrogen species that can damage their basic cell components, which may alter their metabolism. An excessive accumulation of these cell alterations drives macrophages inexorably to cell death, which has been associated to the development of several inflammatory diseases and even with aging in a process termed as "immunosenescence". Macrophages, however, exhibit a prolonged survival in this hostile environment because they equip themselves with a complex network of protective mechanisms. Here we provide an overview of these self-defense mechanisms with special attention being paid to bioactive lipid mediators, NRF2 signaling and metabolic reprogramming.
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页数:9
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