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The power to sense and signal: Mitochondria as stress response modulators

Scientific Conference

Friday 30 January 2015 from 12:00 at 13:00


Martin Picard, PhD

  • CHIR Postdoctoral Fellow, Center for Mitochondrial and Epigenomic Medicine—CMEM, Children’s Hospital of Philadelphia and University of Pennsylvania, Philadelphia

To optimize health care and prevention, we must understand the source of patients’ resilience and vulnerability to biological and psychosocial stress. Therefore, how cells and organs adapt to environmental stressors is a central question to physiology and medicine. Fundamentally, stress adaptation involves energy-dependent cellular processes that remodel gene expression. Sitting at the interface of the plastic (epi) genome and the environment are mitochondria, subcellular organelles containing their own genome – the mitochondrial DNA. In addition to acting as the cell’s powerhouse, an emerging notion suggests that mitochondria i) sense environmental stressors via functional and morphological changes; ii) integrate this information via their physical interactions with each other enabling network behavior, and iii) in turn generate chromatin-modifying biochemical signals that alter gene expression. These three phases of signal transduction are supported by our recent findings in cellular, animal and human disease models, including critical care illness and mechanical ventilation, inherited mitochondrial DNA disorders, psychological stress reactivity, diabetes and aging. This presentation will integrate these recent data into the mitochondrial allostatic load (MAL) model, which provides a framework to decipher the cellular and bioenergetic mechanisms that determine vulnerability to disease.

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Updated on 1/26/2015
Created on 1/26/2015
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