Mitochondrial Dysfunction and COVID-19

Mitochondrial Dysfunction and COVID-19

David Lawrence smiles at the camera

Mitochondria are organelles responsible for the generation of chemical energy in eukaryotic organisms. In humans, our mitochondria are particularly vulnerable when we have infections. Mitochondrial function can also be impacted by exposure to drugs, environmental stressors and comorbidities, such as diabetes and hypertension. These exposures can lead to loss of mitochondrial morphology and function, otherwise known as mitochondrial dysfunction. 

Professor David Lawrence and a partner at the New York State Department of Health Wadsworth Center provided an in-depth report on the various implications of mitochondrial dysfunction with COVID-19 in the Journal of Biochemical and Molecular Toxicology.  

In the article, Lawrence explains that, “during COVID‐19's pathophysiological effects, mitochondria‐rich organs like the brain, muscles, lung, heart, kidney, liver, and the gastrointestinal system in need of more energy are vulnerable, and mitochondrial dysfunction in one or more of these organs may be at high risk for severe COVID‐19 outcomes from combinations of multiple environmental stressors.” 

Simply put, persons with COVID-19 who experience mitochondrial dysfunction may be at risk for poor health outcomes. Thus, Lawrence emphasizes the importance of close monitoring of mitochondrial integrity and function for those diagnosed with COVID-19. Lawrence explains that mitochondrial monitoring is particularly important in populations with health disparities, as there is increased susceptibility to COVID‐19 due to dysfunctional mitochondria. 

“A better understanding of the role of mitochondria during SARS‐CoV‐2 infection may help to improve intervention therapies and better protect patients from pathogens as well as people living with poor nutrition and elevated levels of socioeconomic stress and environmental chemicals,” says Lawrence.