Helmholtz Zentrum München, Institute of Metabolism and Cell Death, 85764 Neuherberg, Germany.
Institute of Bioanalytical Chemistry, Faculty of Chemistry and Mineralogy, University of Leipzig, Leipzig 04013, Germany; Center for Biotechnology and Biomedicine, University of Leipzig, Leipzig 04013, Germany.
Trends Endocrinol Metab. 2021 Jul;32(7):463-473. doi: 10.1016/j.tem.2021.04.012. Epub 2021 May 11.
Lipid peroxidation (LPO) is the molecular mechanism involved in oxidative damage of cellular membranes and the hallmark of a nonapoptotic form of cell death, known as ferroptosis. This iron-dependent cell death is an emerging strategy in cancer treatment and one of the central cell death mechanisms accounting for early cell loss and organ dysfunction in both neurodegenerative disease and ischemia-reperfusion injury. Although the biological roles of LPO products have attracted considerable attention, not only for their pathological mechanisms but also for their potential clinical application as biomarkers, the existence of a common lethal lipid death signal generated during ferroptosis remains poorly explored. A better understanding of the LPO process, however, may unleash unprecedented opportunities for therapeutic intervention of as-yet incurable diseases.
脂质过氧化 (LPO) 是细胞膜氧化损伤涉及的分子机制，也是一种非凋亡形式细胞死亡的标志，称为铁死亡。这种铁依赖性细胞死亡是癌症治疗中的一种新兴策略，也是导致神经退行性疾病和缺血再灌注损伤中早期细胞丢失和器官功能障碍的主要细胞死亡机制之一。尽管 LPO 产物的生物学作用引起了相当大的关注，不仅因为它们的病理机制，还因为它们作为生物标志物的潜在临床应用，但在铁死亡过程中产生的共同致命脂质死亡信号的存在仍未得到充分探索。然而，对 LPO 过程的更好理解可能为治疗目前无法治愈的疾病带来前所未有的机会。
