There's a silent killer coursing through our veins, and we haven't noticed it for decades. It's not the dreaded platelets or the infamous fibrin clots. It is our own red blood cells that, under certain conditions, become microscopic bombs ready to explode. When endothelial cells die, perhaps during a heart attack or a serious infection such as Covid, red blood cells break and transform their membranes into a kind of biological putty. This “cement” seals the damaged vessels, but at the cost of completely blocking circulation. It is as if the body, in an attempt to save itself, ends up strangling itself. And the most disturbing thing? The anticoagulants we normally use against this process are totally ineffective.
A mechanism hidden by a century of medicine
The discovery comes from Shaun Jackson, professor and director of ThromBio, who along with his team analyzed more than 1000 blood vessels from patients who died of COVID-19. What they found shattered a century of medical certainties about clotting.
“We’ve discovered a completely new blood clotting mechanism that has nothing to do with the traditional system involving platelets or fibrin,” Jackson explains. “Instead, dying cells cause red blood cells to explode, and their membranes act like a biological glue, sealing damaged blood vessels and blocking blood flow to vital organs.”
The process is linear: normally, when a vessel gets damaged, platelets aggregate rapidly forming a temporary plug, while a cascade of proteins activates fibrin which creates a stable network to seal the wound. But this new mechanism works differently.
When red blood cells become biological cement
The research team observed that when endothelial cells (the cells that line the inside of vessels) die, they release signals that cause nearby red blood cells to explode. The contents of these “hemolyzed” red blood cells spill into the microcirculation, creating sticky deposits that completely clog the capillaries.
“Under the microscope, we could clearly see deposits of protein-like material at sites of endothelial cell death,” Jackson says. “A closer look revealed that this material was coming from bursting red blood cells, whose sticky contents had spilled out and clogged the microvasculature.”
Research, published in the prestigious magazine Nature, has shown that this phenomenon does not occur only in COVID-19. Tests on animal models have confirmed that the mechanism is also activated during heart attacks, strokes and intestinal ischemia: any condition in which tissues are deprived of oxygen.
Why Anticoagulants Fail
That’s why so many patients with severe COVID developed multiple organ failure despite anticoagulant therapy. “The blood thinners currently used don’t work well on the microvascular clotting of COVID-19 because blood clots aren’t the primary problem,” Jackson says.
It is a revelation that explains many therapeutic failures of the past. As we have highlighted in this article, blood is much more complex than we imagine, and this new mechanism is clear proof of that.
Red Blood Cells: From Transporters to Killers
Traditionally, red blood cells were considered simple oxygen transporters, passive cells without a nucleus whose only job was to shuttle between the lungs and tissues. But Jackson's research shows that have an active and potentially lethal role in coagulation.
When they die, these blood cells don’t simply dissolve. Their membranes act like microscopic drops of superglue, sticking to vessel walls and clumping together to form impenetrable plugs. This mechanism probably evolved to quickly seal wounds, but in pathological conditions it becomes counterproductive.
A new therapeutic era
The discovery opens up entirely new therapeutic avenues. “Rather than targeting platelets or clots, therapies could instead aim to prevent endothelial cell death or block the resulting damage to red blood cells,” Jackson suggests. “By stopping this process early, we may be able to preserve blood flow, protect organs, and ultimately save lives.”
It’s the beginning of what Jackson calls “a whole new chapter in vascular biology.” A chapter that could rewrite emergency protocols for heart attacks, strokes, and all those conditions in which life depends on the ability of blood to continue flowing. Because in the end, the most insidious enemy may not be the one that blocks the vessels from the outside, but the one that destroys them from the inside, drop by drop, blood cell by blood cell.
