For decades, mitochondria were cast in the limited, yet essential role as powerhouse of the cell. Over the past 25 years, this view has evolved 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, which traditionally was blamed on lack of ATP within cells that had mitochondrial dysfunction. However, recent work has outlined a novel conceptual framework for the role of mitochondria in the cellular physiology and how disruptions in signaling are key contributors to disease etiology.

Yet, the mechanistic details are not fully understood of how signals emerging from mitochondria dictate cell fate, function, and disease. The program will cover mechanistic insights into:

(1) how mitochondrial DNA causes inflammation;

(2) how mitochondrial metabolites regulate cellular epigenetics and influence cell fate and function;

(3) how mitochondria-generated reactive oxygen species (ROS) levels are regulated to activate stress response and control cell fate and function

4) how mitochondria contribute to aging and aging-related diseases, including neurodegenerative diseases.

This Keystone Symposia meeting aims to bring together a diverse group of biologists, clinicians, and pharmaceutical scientists to broaden our basic understanding of the role of mitochondria as central signaling hubs in the cell, as well as address whether mitochondria can be targeted for treatment of a variety of conditions including ischemia-reperfusion, hair loss, inflammation, and neurodegeneration. This meeting will support new collaborations geared toward improving understanding and treatment of diseases where mitochondria play critical roles. Attendees will also benefit from training workshops, panel discussions and a career roundtable, enhancing their skills and expertise in the field.