My laboratory’s interest in aging biology arose out of our observation that reactive oxygen species (ROS) could act as endogenous signaling molecules (Sunderesan, et al., Science, 1995). In that initial study, we showed that cells could purposively produce hydrogen peroxide as part of normal receptor-mediated physiological signaling. We, and others, subsequently firmly established this paradigm, and thereby dispelled the widely held notion that oxidants (i.e. free radicals) function within cells solely as stochastic and random damaging agents. These observations may us reevaluate the free radical theory of aging, which at the time was the prevailing explanation as to why we age. This has led us to broadly evaluate how changes in mitochondrial function and metabolism might regulate the aging process. Currently, we are focused on questions involving autophagy, mitochondrial calcium regulation, lysosomal integrity,and senescence. I am also working with my colleagues Bill Chen and Yuan Liu to develop novel therapeutics for a range of age-related diseases. Several of our small molecules are currently in clinical development or clinical trials.