Mitochondrial dysfunction caused by mtDNA damage is involved in many diseases and is likely to be a driving force behind aging and apoptosis [34] . Here, we investigated the systemic alterations of mt protein expressions by using a dataintegrative network analysis. Respiratory-deficient r 0 cells have been studied to characterize retrograde signaling, which is a controlling mechanism of information flow from the mitochondria to the nucleus and cytoplasm [35] , but the systems property of dysfunctional mt state has not been studied extensively. Through network clustering analysis, we discovered that cells respond to pathological conditions by modulating the coordinated expression/transport of mt proteins.