Most exposed to SARS-CoV-2 are dying slowly as study finds SARS-CoV-2 spike protein triggers cardiac fibrogenesis!

COVID-19-News: A new study by researchers from Taipei Medical University, Wan Fang Hospital-Taiwan, and Makiminato Central Hospital in Japan has unveiled alarming findings about the long-term effects of SARS-CoV-2, the virus responsible for COVID-19. This COVID-19 News report explores how the spike protein of the virus may slowly and insidiously lead to heart damage, particularly through a process known as cardiac fibrogenesis. The study sheds light on the mechanisms by which the virus's spike protein activates pathways leading to heart tissue scarring, or fibrosis, even after the acute phase of infection has passed.


Most exposed to SARS-CoV-2 are dying slowly as study finds SARS-CoV-2 spike
protein triggers cardiac fibrogenesis

The Silent Danger of SARS-CoV-2 Exposure
Since the onset of the COVID-19 pandemic, millions have been exposed to the SARS-CoV-2 virus. While many have recovered, a growing number of individuals continue to suffer from long-term health effects, often referred to as "long COVID." Among these effects, heart-related complications have emerged as a significant concern. This new research focuses on how the spike protein of SARS-CoV-2 triggers a harmful process in the heart called cardiac fibrogenesis.
 
The study's key findings suggest that even those who have seemingly recovered from COVID-19 may be at risk of developing long-term heart issues due to the spike protein's impact on heart tissue. The spike protein, which is critical for the virus's entry into human cells, has been shown to initiate a series of cellular responses that lead to the scarring of heart tissue.
 
How the Spike Protein Causes Heart Damage
The spike protein of SARS-CoV-2 plays a crucial role in the virus's ability to infect cells. It binds to the angiotensin-converting enzyme 2 (ACE2) receptors on the surface of various cells, including those in the heart. This interaction is the first step in the virus's entry into cells. However, the spike protein does more than just facilitate viral entry; it also triggers harmful processes within the heart.
 
The study found that when human cardiac fibroblasts (CFs), a type of cell in the heart, were exposed to the spike protein, they began to exhibit behaviors indicative of fibrosis. Fibrosis is the process by which normal, healthy tissue is replaced with scar tissue, which can lead to impaired heart function. The spike protein was shown to enhance the migration of CFs and increase the production of proteins such as collagen 1 and α-smooth muscle actin, both of which are associated with fibrosis.
 
Moreover, the spike protein also increased the production of reactive oxygen species (ROS) within the cells. ROS are harmful molecules that can damage cells and tissues, contributing to the development of fibrosis. Interestingly, while the spike protein increased ROS production, it did not affect the cells' mitochondrial calcium content or morphology, suggesting that its harmful effects are specifically linked to oxidative stress.
 
The Role of NLRP3 Inflammasomes and NF-κB Signaling
A critical aspect of the study was understanding the mechanisms by which the spike protein triggers fibrosis. The researchers focused on two key pathways: the NLRP3 inflammasomes and NF-κB signaling.
 
NLRP3 inflammasomes are components of the immune system that play a role in the body's response to infections. When activated, they can trigger inflammation, which, if uncontrolled, can lead to tissue damage. The study found that the spike protein activates NLRP3 inflammasomes in cardiac fibroblasts, leading to an inflammatory response that contributes to fibrosis.
 
The NF-κB signaling pathway, another crucial player in the immune response, was also found to be activated by the spike protein. NF-κB is a transcription factor that regulates the expression of various genes involved in inflammation and fibrosis. The study showed that blocking NF-κB signaling reduced the fibrotic effects of the spike protein on cardiac fibroblasts, highlighting the pathway's role in this harmful process.
 
The ACE2 Connection
The study also confirmed the critical role of the ACE2 receptor in mediating the spike protein's effects. When the researchers treated the cells with an antibody that neutralizes ACE2, the spike protein's ability to induce fibrosis was significantly reduced. This finding underscores the importance of the ACE2 receptor not only in viral entry but also in the downstream harmful effects of the spike protein on heart tissue.
 
Implications for Long COVID and Beyond
The findings of this study have significant implications for our understanding of long COVID and the potential long-term health risks associated with SARS-CoV-2 infection. Cardiac fibrosis can lead to various heart problems, including arrhythmias, heart failure, and increased risk of sudden cardiac death. The fact that the spike protein alone, independent of the virus, can trigger such processes is concerning and suggests that even individuals who have recovered from COVID-19 could be at risk.
 
Furthermore, the study highlights potential therapeutic targets for preventing or treating COVID-19-related cardiac fibrosis. By targeting the ACE2 receptor, NLRP3 inflammasomes, or NF-κB signaling, it may be possible to mitigate the spike protein's harmful effects on the heart.
 
Thailand Medical News would like to add that while the study did not cover as to whether spike proteins generated by the COVID-19 RNA vaccines would have the similar impact..it seems plausible that these vaccines can also do trigger the same if not worse. Urgent studies are warranted to look into it.
 
Conclusion
In conclusion, this study provides critical insights into how the spike protein of SARS-CoV-2 can trigger cardiac fibrogenesis, leading to long-term heart damage. The research highlights the importance of monitoring individuals who have been exposed to the virus, even if they have recovered from the acute phase of the disease. As we continue to learn more about the long-term effects of COVID-19, studies like this will be crucial in guiding public health strategies and developing treatments to protect those at risk.
 
The study findings were published in the peer-reviewed journal: Cells.
https://www.mdpi.com/2073-4409/13/16/1331
 
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