Mitochondria Signaling in Physiology and Disease

January 1-4, 2026 | Location to be Determined
Scientific Organizers:

  In Person
  On Demand

January 1-4, 2026 | Location to be Determined
Scientific Organizers:

Important Deadlines
Early Registration Deadline:
Scholarship Deadline:
Global Health Award Deadline:
Short Talk Abstract Deadline:
Poster Abstract Deadline:
Meeting Summary

# Biochemistry, Structural and Cellular

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, hair growth, inflammation, and neurodegeneration. These topics will be addressed in this conference that brings a diverse group of biologists, clinicians, and pharmaceutical scientists. We don’t think our meeting is good link for ongoing cancer metabolism or immunometabolism meeting as we have don’t have speakers that address mitochondrial bioenergetics or mitochondria function in metabolism for growth/proliferation. These are main topics covered by those meetings. We are worried their presence will “dwarf” our meeting. If there is an aging meeting, then we could imagine that it could much better link with our conference.

Subscribe for Updates