Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells.

ABSTRACT: Mitochondrial reactive oxygen species (ROS), insufficient NAD⁺, and cellular senescence all contribute to the decrease in bone formation with aging. ROS can cause senescence and decrease NAD⁺, but it remains unknown whether these mechanisms mediate the effects of ROS in vivo. Here, we generated mice with deletion of the mitochondrial antioxidant enzyme Sod2 in Osx1-Cre (Sp7-tTA,tetO-EGFP/cre) targeted cells, designated Sod2^ΔOsx1. We showed that Sod2 deletion caused low bone mass. Osteoblastic cells from these mice had impaired mitochondrial respiration and attenuated NAD⁺ levels. Administration of an NAD⁺ precursor improved mitochondrial function in vitro but failed to rescue the low bone mass of Sod2^ΔOsx1 mice. Single-cell

SUBMITTER: Ali MM 

PROVIDER: S-EPMC12423689 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature