“A recent study presents a groundbreaking revelation about the link between red blood cells and organ damage in deceased COVID-19 patients. The damage was observed to be extensive, influencing endothelial cells that line blood vessels and impacting critical organs such as the lungs, heart, kidneys, and liver. Researchers uncovered protein-like material from ruptured red blood cells clogging the microvasculature, casting new light on a possible novel mechanism that instigates organ damage in severe cases of the disease.
This discovery could pave the way for more focused research on how red blood cells play a role in organ damage, potentially providing fresh insights that could shape effective treatment strategies for severe COVID-19 cases. By fully understanding the function of red blood cells in this process, it may be possible to develop targeted therapies that mitigate organ damage and enhance patient outcomes in the future.
Researchers have identified an unseen biological process that incites tissue and organ damage in conditions characterized by low oxygen levels, such as heart attacks and strokes. Contrary to previous assumptions, the study implies that rupturing red blood cells, rather than blood clots, are the primary culprits in these scenarios.
The microvasculature, a network of minuscule blood vessels vital for oxygen and nutrient delivery to tissues, can be seriously compromised by damage. Disruption to these vessels can lead to life-threatening conditions like heart attacks and strokes. In these conditions, microvascular dysfunction can result in poor blood flow, oxygen deficiency, tissue death, and inflammation, all of which can exacerbate patient outcomes.
A global team of researchers from institutions based in Australia and New York has identified an unprecedented biological process that triggers tissue and organ damage in low-oxygen conditions. This process is driven by red blood cells and not by the blood clots traditionally associated with such damage.
According to Professor Shaun Jackson, founder and director of ThromBio, “We’ve discovered a completely new blood-clotting mechanism that has nothing to do with the traditional clotting system involving platelets or fibrin. Instead, dying cells cause red blood cells to burst, and their membranes act like a biological glue – sealing off damaged blood vessels and blocking blood flow to vital organs.”
Traditionally, when a blood vessel is injured, tiny cell fragments called platelets quickly adhere to the damaged site and one another, forming a temporary plug. Simultaneously, a cascade of proteins in the blood activates the protein fibrin, which forms a mesh that stabilizes the platelet plug, creating a robust and lasting clot to seal the vessel and stop bleeding.
Researchers initially believed that both acute and long COVID infections could damage the body’s tiny blood vessels, making it harder for blood to circulate properly. Excessive fibrin was thought to be the culprit, but treatment with blood thinners to clear the fibrin yielded little benefit. This led the researchers to investigate an alternative cause, leading to the discovery of this new, red blood cell-driven mechanism.”
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