BREAKING! SARS-CoV-2 Encodes Circular RNAs That Can Impair Endothelial Cells and Cause Cardiovascular Issues!
Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 13, 2025 3 hours, 36 minutes ago
Medical News: Scientists Discover a New Threat from SARS-CoV-2
In a groundbreaking study, researchers have unveiled a previously unknown ability of the SARS-CoV-2 virus - the ability to encode circular RNAs (circRNAs) that can harm endothelial and heart cells. This shocking revelation raises new concerns about the long-term cardiovascular effects of COVID-19. Scientists from South China University of Technology, Guangdong Provincial People’s Hospital, Guangzhou Medical University, Guangdong Provincial Center for Disease Control and Prevention, and Guangdong Cardiovascular Institute have collaborated to uncover the hidden mechanisms by which these viral circRNAs contribute to heart and vascular damage.
SARS-CoV-2 Encodes Circular RNAs That Can Impair Endothelial Cells and Cause
Cardiovascular Issues!
Understanding the Role of Circular RNAs in Viral Infections
Circular RNAs are a unique type of noncoding RNA that form covalently closed loops, making them highly stable and capable of influencing gene expression.
While circRNAs have been previously studied in human biology, the presence of virus-derived circRNAs is a relatively new discovery. This
Medical News report highlights that SARS-CoV-2 can produce various circRNAs, particularly from its nucleocapsid (N) gene, which may play a significant role in the virus’s impact on cardiovascular health.
Among the identified circRNAs, circSARS-CV2-N1368 stands out due to its ability to impair endothelial function, increasing the likelihood of heart complications in infected individuals. The study’s findings demonstrate that this circRNA contributes to increased platelet adhesion, oxidative stress, and vascular inflammation, ultimately leading to cardiovascular dysfunction.
The Mechanism Behind the Damage
Researchers have determined that circSARS-CV2-N1368 exerts its effects by interacting with a specific microRNA (miRNA), miR-103a-3p. Normally, miR-103a-3p helps regulate endothelial cell function and reduces inflammation. However, circSARS-CV2-N1368 acts as a "sponge" for this miRNA, preventing it from performing its protective role.
Without sufficient levels of miR-103a-3p, endothelial cells experience increased expression of a protein called activating transcription factor 7 (ATF7), which in turn activates the Toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) pathways. This chain reaction leads to excessive production of reactive oxygen species (ROS), causing oxidative stress and damage to the blood vessel lining. The result is an increased risk of blood clotting, inflammation, and endothelial dysfunction, all of which can contribute to cardiovascular complications seen in many COVID-19 patients.
Real-World Implications for Cardiovascular Health
These findings shed new light on why COVID-19 patients often suffer from vascular complications such as blood clots, strokes, and heart disease. The ability of
SARS-CoV-2 to encode circRNAs that disrupt endothelial cell function provides a potential explanation for the lingering cardiovascular issues observed in long COVID patients.
The study also provides a potential therapeutic target. Researchers found that when they introduced a ROS scavenger called N-acetylcysteine (NAC), it significantly reduced oxidative stress and reversed the harmful effects of circSARS-CV2-N1368 on endothelial cells. This suggests that antioxidant treatments could be a viable approach to mitigate SARS-CoV-2-induced cardiovascular damage.
Further Research and Potential Treatments
Given the critical implications of these findings, further research is needed to explore how widespread the production of viral circRNAs is across different SARS-CoV-2 variants. Scientists also aim to determine whether these circRNAs persist long after initial infection, potentially contributing to long COVID symptoms.
One promising avenue for future treatments involves developing targeted therapies that can prevent circSARS-CV2-N1368 from interacting with miR-103a-3p. By blocking this interaction, researchers may be able to prevent the activation of the ATF7/TLR4/NF-κB pathway and reduce oxidative stress in endothelial cells. This could help lower the risk of cardiovascular complications in COVID-19 patients and long-haulers.
Conclusion: A New Frontier in Understanding COVID-19’s Impact
This research marks an important step in understanding how SARS-CoV-2 contributes to cardiovascular disease. By identifying circSARS-CV2-N1368 as a key player in endothelial dysfunction, scientists have opened new doors for potential treatments aimed at mitigating the long-term effects of COVID-19.
With cardiovascular complications becoming an increasing concern for COVID-19 survivors, it is crucial to continue exploring the full impact of SARS-CoV-2 on the human body. Future studies may reveal additional viral circRNAs that play roles in other organ systems, further expanding our knowledge of the virus’s far-reaching effects.
The study findings were published in the peer-reviewed journal: Acta Pharmacologica Sinica.(Nature)
https://www.nature.com/articles/s41401-025-01516-8
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