Mitochondrial Damage and RAAS Overactivation in Severe COVID-19
mitochondrial Damage May Fuel Severe COVID-19, Study Suggests
new research points to a potential culprit behind the devastating effects of severe COVID-19: damage to mitochondria, the tiny powerhouses within our cells.
Scientists from leading institutions, including Weill Cornell Medicine and Johns Hopkins Medicine, have uncovered a chain reaction triggered by SARS-CoV-2 infection that could explain the organ damage and immune system overdrive seen in severe cases.
While severe COVID-19 has been characterized by an overwhelming “cytokine storm” – an excessive immune response flooding the body wiht inflammatory proteins – this new study suggests a deeper, more fundamental cause.
The researchers found that SARS-CoV-2 infection can substantially damage mitochondria in infected cells. This damage, in turn, activates the immune system, contributing to the inflammatory storm.
One key consequence of this mitochondrial damage is the overactivation of the renin-angiotensin-activation-system (RAAS), a system that regulates blood pressure. This overactivation is linked to abnormal blood clotting, a hallmark of severe COVID-19, as well as scarring in lymph nodes and dysfunction of immune cells within them.
“These findings suggest that early on in the infection process, ther’s profound mitochondrial dysfunction and damage,” explains Dr. Schwartz, a hepatologist at NewYork-Presbyterian/Weill Cornell Medical Center. “This damage drives RAAS overactivation, wich contributes to the multi-organ damage seen in severe COVID-19.”
Long-Term Implications
The researchers are now investigating whether these processes underlying acute COVID-19 can have lasting effects, potentially contributing to “long COVID,” a syndrome marked by persistent inflammation and immune dysfunction.
This groundbreaking research sheds new light on the complex mechanisms behind severe COVID-19 and opens up potential avenues for developing targeted therapies that address mitochondrial damage and RAAS overactivation.
Mitochondrial Damage may Be Key Driver of Severe COVID-19, Study Suggests
New research published by scientists from Weill Cornell Medicine and Johns Hopkins medicine points too a potential culprit behind the devastating effects of severe COVID-19: damage to mitochondria, the powerhouses of our cells.
While severe COVID-19 has been characterized by a damaging “cytokine storm” – an overactive immune response, this new study suggests a more fundamental cause. The researchers found that SARS-CoV-2 infection can cause ample damage to mitochondria in infected cells. This damage, in turn, triggers the immune system, contributing to the inflammatory storm.
Dr.Schwartz, a hepatologist at NewYork-Presbyterian/Weill Cornell Medical Center, explains, “These findings suggest that early on in the infection process, there’s profound mitochondrial dysfunction and damage.This damage drives RAAS overactivation, which contributes to the multi-organ damage seen in severe COVID-19.”
One critical result of this mitochondrial damage is the overactivation of the renin-angiotensin-activation-system (RAAS),a system that regulates blood pressure. This overactivation is linked to abnormal blood clotting, a common feature of severe COVID-19, as well as scarring in lymph nodes and dysfunction of immune cells within them.
The researchers are now investigating whether these processes behind acute COVID-19 can have long-term effects, potentially contributing to Long COVID, a syndrome marked by persistent inflammation and immune dysfunction.
This groundbreaking research shines a light on the complex mechanisms behind severe COVID-19 and paves the way for the development of targeted therapies that address mitochondrial damage and RAAS overactivation.