COVID-19’s hidden impact: Unmasking Mitochondrial Dysfunction across organ systems
Since the emergence of COVID-19, researchers have been perplexed by its enduring effects
A collaborative study by the Children’s Hospital of Philadelphia (CHOP) and the COVID-19 International Research Team (COV-IRT) uncovers a critical puzzle piece: the virus triggers mitochondrial dysfunction, leading to multi-organ complications.
How Mitochondria Dysfunction respond to COVID-19
Mitochondria, the cell’s energy producers, house genetic information in nuclear and mitochondrial DNA (mtDNA). Notably, SARS-CoV-2 proteins show an affinity for mitochondrial proteins, raising suspicions of mitochondrial impairment.
Researchers from CHOP’s Center for Mitochondrial and Epigenomic Medicine (CMEM) partnered with COV-IRT to explore how the virus affects mitochondrial gene expression across various organs.
Unmasking the prolonged impact beyond the lungs
A comprehensive analysis of human samples and animal models yielded intriguing findings. While lung mitochondria regained function, the heart, liver, and kidneys continued to suffer from virus-induced dysfunction.
Remarkably, even the cerebellum experienced mitochondrial gene expression suppression, despite the virus’s absence from the brain. Through animal models, researchers observed a gradual recovery of lung mitochondrial function coinciding with the virus’s peak.
A paradigm shift in understanding COVID-19
From respiratory to systemic disorder with lasting consequences, this study redefines the narrative around COVID-19, unearthing its systemic nature and enduring impact on various organs. Persistent mitochondrial dysfunction, particularly in the heart, highlights the potential for long-term internal harm.
The study also identifies a possible intervention target: microRNA 2392 (miR-2392), elevated in the blood of COVID-19 patients, offering a potential means to impede viral replication.
Illuminating new pathways for treatment
This breakthrough study sheds light on the intricate relationship between COVID-19 and mitochondrial dysfunction, stretching beyond pulmonary complications and unraveling the origins of long COVID.
As investigations delve deeper into immune and inflammatory responses, the identified microRNA 2392 emerges as a promising avenue for therapeutic intervention.
The study’s findings not only expand upon the Gates Foundation’s support for mitochondrial research but also fuel the hypothesis that individual mitochondrial function could influence COVID-19 severity.
This work underscores the complex landscape of the pandemic’s aftermath and introduces innovative treatment possibilities.
