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eBriefing

The Role of Mitochondria in Complex Diseases

The Role of Mitochondria in Complex Diseases
Reported by
Alison Carley and Barbara Knappmeyer

Posted June 02, 2020

Presented By

The New York Academy of Sciences

The canonical role of mitochondria is to function as the key regulator of cellular energy metabolism. However, mitochondria also play wider roles in cellular signaling, differentiation, cell death, regulation of the cell cycle and cell growth, in reactive oxygen species generation, and regulation of the epigenome. Dysregulation of these processes contribute to the aging process and play key roles in pathologies such as cancer, neurodegeneration, inflammatory and auto-immune diseases, and cardiovascular disease. While there have been advances in our understanding of basic mitochondrial biology and how the organelle regulates diverse cellular processes in recent years, the full implications of mitochondrial damage and dysfunction on human health and longevity are unknown.

The New York Academy of Sciences’ conference Mitochondria in Complex Diseases, held virtually on April 21, 2020, shed light on the impact of these cellular powerhouses in physiology and medicine. Speakers explored new advances in the basic biology of mitochondria, as well as the role of mitochondrial damage and dysfunction in cardiovascular disease, immunology, regenerative medicine, neurodegenerative disease, and aging.

“This meeting could not be timelier, as the globe deals with effects of the global COVID-19 pandemic," said scientific organizing committee member Douglas C. Wallace, PhD. "While it has been known for some time that viruses interact with certain aspects of mitochondrial function, SARS-CoV and SARS-CoV2 have brought the importance of the mitochondria in viral pathogenesis into sharp focus," he continued. "Analysis of the recent characterization of interactions of SARS-CoV2 proteins with cellular proteins has revealed the striking extent to which the viral non-structural protein and open reading frame polypeptides directly interact with our mitochondria and the systems that communicate the mitochondrial bioenergetic status to the rest of the cell.”

In this eBriefing you will learn:

  • New advances in mitochondrial disease mechanisms
  • New concepts in the pathophysiology of human mitochondrial disease as well as therapeutic interventions
  • How mitochondrial dysfunction plays a role in cardio metabolic disease, neurodegeneration, and cancer
  • New therapeutic techniques for altering mitochondrial function
Keynote: Mitochondrial Dynamics and Cardiometabolic Disease
Imbalances in Type I Interferon and Nrf2 Signaling Drive Myeloid Reprogramming and Tissue Dysfunction in a Model of Mitochondrial DNA Disease
Mitochondrial Dynamics in the Regulation of Neurogenesis

Ruth Slack, PhD
University of Ottawa Brain and Mind Research Institute

Dr. Ruth Slack is Professor of Cellular and Molecular Medicine and Vice-Dean at the University of Ottawa. Her research group’s long-term goals are to promote the regeneration of the damaged brain after stroke or in neurodegenerative diseases. She and her team have shown that proteins that regulate cell replication can also play important roles in the regulation of neural stem cell self-renewal and long term maintenance in the embryonic and adult brain. Dr. Slack’s group has also shown that mitochondrial dynamics and function have a major impact on adult stem cells and their differentiation, thus changes in metabolism or defects in mitochondrial function in the context of neurodegenerative diseases may have a major impact on neurogenesis, regeneration and neurological function. By exploiting new knowledge of these key regulatory pathways, they plan to activate the neuronal precursor and stem cell pools in order to facilitate regeneration of the damaged brain.

Mitochondrial Dynamics in the Regulation of Neurogenesis


Ruth Slack, PhD (University of Ottawa Brain and Mind Research Institute)

Further Readings

The Role of Mitochondrial Dynamics in Tissue Stem Cells
Mitochondrial Dysfunction as a Consequence of Nuclear DNA Damage
Mitochondria Contact Sites in Neurodegeneration
Mitochondrial Division and Cancer: Causes, Consequences, and Coincidence
Closing Remarks