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Updated: Jan 25, 2026

Techniques to Induce and Quantify Cellular Senescence
Published on: May 1, 2017
Vitisin B rejuvenates senescence via WBP2NL regulation
Jee Hee Yoon1, Yun Haeng Lee1, Sekyung Oh2
1Division of Life Sciences, College of Life Sciences and Bioengineering, Incheon National University, Incheon 22012, Republic of Korea.
None:
One of the main factors contributing to aging is reactive oxygen species (ROS), which are produced by dysfunctional mitochondria. Reducing ROS generation is considered an essential treatment for senescence, but no effective treatment has been developed yet. In this study, vitisin B, a tetramer of resveratrol, was found to be an efficient reagent that reduces mitochondrial ROS generation after screening phenylpropanoids (PPs), metabolites produced to overcome ROS-mediated stress in plants. Vitisin B induced mitochondrial functional recovery by activating mitophagy and removing dysfunctional mitochondria. Mitochondrial functional recovery by vitisin B decreased mitochondrial ROS, a by-product generated from dysfunctional mitochondria. In addition, ROS reduction by vitisin B restored senescence-associated phenotypes. RNA sequencing identified WBP2 N-Terminal Like (WBP2NL) as a gene essential for vitisin B-mediated senescence rejuvenation. Knockdown of WBP2NL exhibited effects similar to those of vitisin B, reducing mitochondrial ROS generation and consequently reversing senescence-associated phenotypes. This study elucidates a novel mechanism by which vitisin B reverses senescence by lowering mitochondrial ROS generation. This discovery opens the way to new therapeutic options to control aging by modulating mitochondrial ROS production.
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