Pedroza-Diaz Johanna, Arroyave-Ospina Johanna C, Serna Salas Sandra, Moshage Han
University Medical Center Groningen, Department of Gastroenterology and Hepatology, University of Groningen, 9712 CP Groningen, The Netherlands.
Grupo de Investigación e Innovación Biomédica GI2B, Facultad de Ciencias Exactas y Aplicadas, Instituto Tecnológico Metropolitano, Medellín 050536, Colombia.
Antioxidants (Basel). 2022 May 16;11(5):975. doi: 10.3390/antiox11050975.
Non-alcoholic fatty liver disease is characterized by disturbed lipid metabolism and increased oxidative stress. These conditions lead to the activation of different cellular response mechanisms, including senescence. Cellular senescence constitutes an important response to injury in the liver. Recent findings show that chronic oxidative stress can induce senescence, and this might be a driving mechanism for NAFLD progression, aggravating the disturbance of lipid metabolism, organelle dysfunction, pro-inflammatory response and hepatocellular damage. In this context, the modulation of cellular senescence can be beneficial to ameliorate oxidative stress-related damage during NAFLD progression. This review focuses on the role of oxidative stress and senescence in the mechanisms leading to NAFLD and discusses the possibilities to modulate senescence as a therapeutic strategy in the treatment of NAFLD.
非酒精性脂肪性肝病的特征是脂质代谢紊乱和氧化应激增加。这些情况会导致不同细胞反应机制的激活，包括细胞衰老。细胞衰老构成肝脏对损伤的重要反应。最近的研究结果表明，慢性氧化应激可诱导衰老，这可能是NAFLD进展的驱动机制，加剧脂质代谢紊乱、细胞器功能障碍、促炎反应和肝细胞损伤。在这种情况下，调节细胞衰老可能有助于改善NAFLD进展过程中与氧化应激相关的损伤。本综述重点关注氧化应激和衰老在导致NAFLD的机制中的作用，并讨论将调节衰老作为NAFLD治疗策略的可能性。
