Mitochondria are dynamic organelles that are essential for energy production and cellular processes in eukaryotic cells, and their functional failure is a major cause of ageassociated degenerative diseases. To meet the specific needs of different cellular states, mitochondrial protein repertoires are adjusted. It is critical to characterize the systemic alterations of mitochondria to different cellular states to understand the dynamic organization of mitochondrial systems. In this study, we modularized the quantified proteomics data into protein functional networks to characterize gene expression changes under dysfunctional mitochondrial conditions. Our results demonstrate that mitochondrial protein repertoires changed to compensate for dysfunctional cellular states by reorganizing mitochondrial protein functional network. Through network clustering analysis, we discovered that cells respond to pathological conditions by modulating the coordinated expression/transport of mitochondrial proteins. Network analysis of mt proteins can advance our understanding of dysfunctional mitochondrial systems and elucidate the candidate mt proteins involved in human mitochondrial diseases.