Reactive oxygen species (ROS) operate as key regulators of cellular homeostasis within a physiological range of concentrations, yet they turn into cytotoxic entities when their levels exceed a threshold limit. Accordingly, ROS are an important etiological cue for obesity, which in turn represents a major risk factor for multiple diseases, including diabetes, cardiovascular disorders, non-alcoholic fatty liver disease, and cancer. Therefore, the implementation of novel therapeutic strategies to improve the obese phenotype by targeting oxidative stress is of great interest for the scientific community. To this end, it is of high importance to shed light on the mechanisms through which cells curtail ROS production or limit their toxic effects, in order to harness them in anti-obesity therapy. In this review, we specifically discuss the role of autophagy in redox biology, focusing on its implication in the pathogenesis of obesity. Because autophagy is specifically triggered in response to redox imbalance as a quintessential cytoprotective mechanism, maneuvers based on the activation of autophagy hold promises of efficacy for the prevention and treatment of obesity and obesity-related morbidities.

中文翻译：

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靶向自噬以抵消肥胖相关的氧化应激

活性氧（ROS）在浓度范围内可作为细胞稳态的关键调节剂，但当其含量超过阈值极限时，它们就会变成细胞毒性实体。因此，ROS是肥胖的重要病因学线索，其又代表多种疾病的主要危险因素，包括糖尿病，心血管疾病，非酒精性脂肪肝疾病和癌症。因此，通过靶向氧化应激来改善肥胖表型的新型治疗策略的实施对于科学界非常重要。为此，阐明细胞减少ROS产生或限制其毒性作用的机制，以利用它们进行抗肥胖治疗非常重要。在这篇评论中 我们专门讨论自噬在氧化还原生物学中的作用，重点是其在肥胖发病机理中的意义。由于自噬是作为一种典型的细胞保护机制而响应于氧化还原失衡而特别触发的，因此基于自噬激活的操纵有望有效预防和治疗肥胖症和与肥胖相关的疾病。