For decades, mitochondria were cast in the limited, yet essential role as powerhouse of the cell. In the past 25 years, this view has changed as mitochondria have emerged as a major signaling hub that dictates cellular fate and function to control cellular physiology. Aberrant mitochondrial signaling can cause diseases and for the longest time the common perception of the etiology of mitochondrial disease was a lack of ATP within cells that had mitochondrial dysfunction. Recent work outlined novel conceptual framework for the role of mitochondria in the cellular physiology, yet, the mechanistic details are not fully understood of how signals emerging from mitochondria dictate cell fate and function. These include (1) how mtDNA, known to cause inflammation, is released from mitochondria into the cytosol; (2) how mitochondrial metabolites control epigenetics; (3) how mitochondria ROS levels are regulated and control cell function and fate by cysteine oxidation; 4) what mitochondria dependent mechanisms control neurodegenerative diseases; 5) how mitochondria integrate to activate stress responses; 6) which mitochondrial metabolites control cell fate and function. Beside these questions aimed to broaden our basic understanding of the role of mitochondria as central signaling hub in the cell, the conference will address whether mitochondria can be targeted for variety of diseases including ischemia-reperfusion, inflammation, and neurodegeneration as well as aging. These topics will be addressed in this conference that brings a diverse group of biologists, clinicians, and pharmaceutical scientists.