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Here, as an additional perspective to overviews associating excessive ROS production with oxidative stress as previously put forward [1,2], we concentrate on the necessity for ROS-S systems, with a focus upon some of their crucial roles in normal endocrine cardio-metabolic physiology

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H 2 O 2 directly oxidizes the Cys81 of Atg4 (Scherz-Shouval et al., 2007), thus leading to the inactivation of Atg4 and promoting the lipidation of light chain 3 (LC3, also the mammalian homolog of Atg8), thereby supporting the formation of autophagosomes (Prez-Prez et al., 2021)

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