Study Unveils Surprising Competition Between SARS-CoV-2 and Epithelial Sodium Channel for Plasmins.
COVID-19-News - SARS-CoV-2 - Epithelial Sodium Channel - Plasmins Jun 01, 2023 1 year, 5 months, 3 weeks, 19 hours, 47 minutes ago
COVID-19 News: In a groundbreaking study conducted by researchers at the China Medical University in Shenyang, China, a fascinating discovery has been made regarding the interaction between SARS-CoV-2, the virus responsible for COVID-19, and the epithelial sodium channel (ENaC) in the lungs. The study reveals a surprising competition between the virus and ENaC for plasmins, which has significant implications for our understanding of the disease and potential treatment strategies.
One of the key clinical features of COVID-19 is the development of dyspnea and progressive hypoxemia in affected patients. The pulmonary pathology observed in COVID-19 patients aligns with the criteria for Acute Respiratory Distress Syndrome (ARDS), characterized by diffuse alveolar damage, edema, hemorrhage, and the deposition of fibrinogens in the alveolar space. ENaC, a crucial channel protein involved in alveolar ion transport and fluid clearance, plays a vital role in regulating pulmonary edema. Dysregulation of ENaC has been linked to the development of acute lung injury and ARDS.
Plasmin, the primary protein in the fibrinolysis system, has the ability to bind to the furin site of γ-ENaC, inducing its activation and facilitating the reabsorption of pulmonary fluid. Interestingly, the spike protein of SARS-CoV-2 contains the same furin site as ENaC, suggesting a potential competition between the virus and ENaC for plasmin cleavage.
This competition could explain why ENaC is downregulated in COVID-19 patients and why pulmonary edema is observed in severe cases.
Past studies and
COVID-19 News reports have already indicated that COVID-19 patients frequently exhibit extensive pulmonary microthrombosis, indicating disruptions in the coagulation and fibrinolysis system. High levels of plasmin (ogen) have been identified as a common risk factor for SARS-CoV-2 infection, as increased cleavage by plasmin accelerates virus invasion.
These study findings suggest that COVID-19 is not solely a respiratory disease but also a systemic thrombotic condition, emphasizing the need to address the underlying coagulation and fibrinolysis dysfunctions in treatment approaches.
The unique furin site found in the spike protein of SARS-CoV-2, along with its variants, enhances the cleavability of the virus and promotes viral invasion into host cells. By investigating the regulation of ENaC and its association with fibrinolysis system-related proteins, the study team have shed light on the intricate relationship between SARS-CoV-2 and ENaC. This understanding opens up new avenues for exploring novel treatment strategies for COVID-19 by focusing on sodium transport regulation in lung epithelial cells.
The study also highlights the impact of various factors on ENaC regulation and function during SARS-CoV-2 infection. These factors include the presence of furin, the subcellular localization of ENaC, the role of TMPRSS2 in modulating ENaC expression, and the influence of pro-inflammatory mediators on ENaC activity.
Understanding these mechanisms is crucial for deciphering the pathogenesis of COVID-19 and developing targeted therapies to mitigate the disease's effects.
The implications of this study are far-reaching. Not only does it deepen our understanding of the complex interplay between SARS-CoV-2 and th
e host's physiological processes, but it also offers potential avenues for therapeutic interventions. By focusing on the regulation of sodium transport in the lungs, researchers may uncover novel approaches to enhance pulmonary fluid clearance and alleviate the respiratory distress experienced by COVID-19 patients.
The study findings were published in the peer reviewed journal: Biomolecules.
https://www.mdpi.com/2218-273X/13/4/578
For the latest
COVID-19 News, keep on logging to Thailand Medical News.
Share
Tweet
Share
