Nikhil Prasad Fact checked by:Thailand Medical News Team Jan 11, 2025 3 hours, 7 minutes ago
Medical News: Renin Angiotensin System in Severe COVID-19 Cases
Recent scientific discoveries shed light on the devastating impacts of COVID-19 on the human body. A groundbreaking study involving researchers from the University of Pittsburgh, Children’s Hospital of Philadelphia, Johns Hopkins University, and other leading American institutions has revealed a complex interplay between the immune system and the renin-angiotensin-aldosterone system (RAAS), contributing to multi-organ damage in severe COVID-19 cases. This
Medical News report delves into the study’s findings, presenting the insights in an accessible manner for everyone.
RAAS Activation Causes Widespread Organ Damage in Severe COVID-19
The Link Between Cytokine Storms and RAAS Overactivation
COVID-19 has claimed millions of lives, and severe cases often result in what is termed a "cytokine storm" - an overwhelming inflammatory response that causes significant harm. However, researchers now suggest that this storm is closely linked to RAAS overactivation. RAAS, a critical system in regulating blood pressure and fluid balance, appears to be disrupted by severe SARS-CoV-2 infections.
This article highlights findings from the study, which used RNA sequencing from nasal swabs and 40 autopsy samples, uncovering that RAAS-related genes are hyperactivated in vital organs such as the lungs, heart, kidneys, and liver. Notably, mediastinal lymph nodes - key immune hubs - were heavily impacted, showing signs of fibrosis and reduced function. These alterations are hypothesized to weaken the body’s ability to combat infections effectively, contributing to fatal outcomes.
Exploring RAAS Disruption in Depth
RAAS overactivation in COVID-19 leads to several damaging effects, including:
-Increased Fibrin Deposition: Fibrin is essential for blood clotting, but excessive levels can result in blockages and tissue damage. The study revealed elevated fibrin-producing gene activity in lungs and heart tissues.
-Mitochondrial Dysfunction: SARS-CoV-2 appears to impair mitochondria - the cell’s powerhouse - resulting in increased production of reactive oxygen species (ROS). This mitochondrial stress further triggers inflammation and cell death mechanisms, known as PANoptosis.
-Lymph Node Fibrosis: Mediastinal lymph nodes showed significant architectural changes, with fibrosis impairing their ability to support immune responses. Pathogenic fibroblasts were identified as contributors to this process.
-Bradykinin Storms: Bradykinin, a peptide involved in inflammation, was found to be elevated in severe cases. This led to leaky blood vessels and swelling, compounding organ dysfunction.
Broader Implications for Long COVID
The study’s authors noted potential links between RAAS disruption
and long COVID symptoms. Chronic B and T cell dysfunctions, resulting from lymph node damage, may explain prolonged immune system irregularities in some patients. Insights from these findings could guide treatments targeting RAAS pathways to alleviate long COVID symptoms.
Comparative Findings Across Variants and Models
Analyzing tissues from different COVID-19 variants and infected animal models, the researchers observed consistent patterns of RAAS-related damage. Peripheral blood samples from individuals infected with earlier and later variants showed similar immune responses, reinforcing the hypothesis that RAAS overactivation is a universal feature of severe COVID-19.
Conclusions and Future Directions
This comprehensive study highlights the intricate role of RAAS in COVID-19 pathogenesis, reshaping how researchers understand severe cases. By pinpointing RAAS-related mechanisms such as excessive fibrin deposition, mitochondrial stress, and lymph node fibrosis, the study provides a roadmap for developing targeted interventions.
Future research should focus on therapies that mitigate RAAS overactivation without compromising its essential functions. Such treatments could reduce the severity of organ damage, improve survival rates, and possibly address long COVID symptoms. Understanding how SARS-CoV-2 disrupts RAAS also opens avenues for addressing other diseases involving similar pathways, offering hope for broader medical advancements.
The study findings were published in the peer-reviewed journal: Proceedings of the National Academy of Sciences (PNAS).
https://www.pnas.org/doi/10.1073/pnas.2401968121
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https://www.thailandmedical.news/articles/coronavirus
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