Study Links Severe COVID Deaths To Cell Damage And Inflammation

According to the study, the combined effect of mitochondrial dysfunction and RAAS overactivation triggers the cytokine storm that leads to severe outcomes.

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Updated on: 5 December 2024 10:37 am

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Study Links Severe COVID Deaths To Cell Damage And Inflammation

A recent study has identified mitochondrial dysfunction as a potential driver of organ damage and death in severe COVID-19 cases. Mitochondria, known as the cell's "energy factories," play a critical role in cellular function. Damage or stress to these organelles can trigger immune responses that contribute to excessive inflammation, known as a 'cytokine storm,' which is commonly observed in severe COVID-19 patients. This process not only exacerbates the disease but may also explain long-term complications in survivors, including long COVID.

Researchers highlighted the role of the renin-angiotensin-aldosterone system (RAAS), a network of hormones, proteins, and enzymes essential for regulating blood pressure. When mitochondria are disrupted, they can over activate RAAS, initiating a chain of harmful processes that result in organ damage. This overactivation, combined with mitochondrial stress, intensifies an immune response that spirals out of control, worsening the condition of severe COVID-19 patients.

The findings, published in the Proceedings of the National Academy of Sciences, underscore how these interconnected biological processes drive severe outcomes and may contribute to lingering symptoms in survivors. "Notably, we also found that activation of RAAS caused substantial damage to the lymph nodes, which hasn’t been shown in COVID-19 before," said Professor Afshin Beheshti, co-senior author of the study and a researcher at the University of Pittsburgh. Lymph nodes, a vital component of the immune system, were significantly damaged in these patients, potentially contributing to the prolonged immune dysfunction seen in long COVID cases.

The researchers conducted the study by analyzing autopsy samples from 40 patients who succumbed to COVID-19. These samples, collected from multiple organs including the nasal cavity, lungs, heart, and liver, revealed increased activity in around 50 immune-related genes. The nasal cavity samples, in particular, showed heightened immune gene expression, suggesting that immune system dysregulation starts early and affects various parts of the body.

According to the study, the combined effect of mitochondrial dysfunction and RAAS overactivation triggers the cytokine storm that leads to severe outcomes. "Our study resolves some of the long-standing unanswered questions about how the SARS-CoV-2 virus impacts the body," Beheshti explained. He further noted that these findings point to potential therapeutic approaches to mitigate severe disease and reduce the risk of long COVID.

This research provides critical insights into the mechanisms underlying severe COVID-19 and its aftermath. By identifying the roles of mitochondrial dysfunction and RAAS overactivation, the study offers new avenues for developing treatments that could prevent or alleviate these life-threatening complications, offering hope for improved patient outcomes in the future.

(This article is a reworked version of a PTI feed)