Sauchinone Ameliorates Senescence Through Reducing Mitochondrial ROS Production.

One of the major causes of senescence is oxidative stress caused by ROS, which is mainly generated from dysfunctional mitochondria. Strategies to limit mitochondrial ROS production are considered important for reversing senescence, but effective approaches to reduce them have not yet been developed. In this study, we screened the secondary metabolites that plants produce under oxidative stress and discovered sauchinone as a potential candidate. Sauchinone induced mitochondrial function recovery, enabling efficient electron transport within the electron transport chain (ETC). This led to a decrease in ROS production, a byproduct of inefficient electron transport. The reduction in ROS by sauchinone rejuvenated senescence-associated phenotypes. To understand the underlying mechanism by which sauchinone rejuvenates senescence, we carried out RNA sequencing and found as a key gene. was downregulated by sauchinone. Knockdown of decreased mitochondrial ROS levels and subsequently rejuvenated mitochondrial function, which was similar to the effect of sauchinone. Taken together, these studies revealed a novel mechanism by which sauchinone reduces mitochondrial ROS production by regulating mitochondrial function and expression. Our results open a new avenue for aging research to control senescence by regulating mitochondrial ROS production.