A Novel Strategy to Restore Mitochondrial Function in Aging
Decline in mitochondrial function is a hallmark of aging that is triggered by the accumulation of toxic metabolites, particularly reactive oxygen species (ROS). Approximately 90% of these toxic ROS molecules found in cells come from the electron transport chain (ETC), which is a series of electron transfer reactions that are inside the mitochondria. Although decline in mitochondrial function and accumulation of ROS are well established, little is known about the mechanisms driving changes in the ETC during aging that may cause these phenomena. The proposed research will address this fundamental gap in knowledge using high resolution mass spectrometry to comprehensively elucidate which mitochondrial functions in the ETC decline in mouse tissues during aging. Moreover, we will test a novel strategy to reprogram the ETC and mitochondrial function to mitigate ROS production and mitochondrial decline during aging.
