 MAVS is essential for driving antiviral response and protecting against mitochondrial dysfunction and cellular senescence. It does so by interacting with the OPA1 protein, which helps maintain mitochondrial structure and function. When MAVS or OPA1 are depleted, mitochondrial dysfunction occurs, leading to accelerated senescence in human mesenchymal stem cells. Replenishing either MAVS or OPA1 can reverse these effects and restore normal mitochondrial function. This article was authored by Cui Wang, Quan Yang, Xiao Qianlu, and others.