Atherosclerosis can accelerate the development of clonal hematopoiesis

Billions of peripheral white blood cells are produced daily by regularly dividing hematopoietic gas cells and their offspring in the bone marrow. Under normal circumstances, thousands of cells attach a gene to the blood at any given time, making white blood cells a group with diverse ancestry.

Clonal hematopoiesis is a common age-related condition in which the offspring of one of these hematopoietic cells begin to dominate large parts of the blood. Genome-wide analyzes have shown that clonal hematopoiesis is often driven by recurrent genetic changes that give specific hematopoietic gas cells a competitive advantage, thus enabling them to proliferate unevenly.

Multiple independent studies have shown that clonal hematopoiesis is often associated with atherosclerosis and cardiovascular disease. Since its discovery, this remarkable connection has been the subject of great interest from both clinicians and researchers alike.

Cardiovascular disease is a major cause of morbidity and mortality in Western countries and represents a major burden on public health. Does clonal dilation in the blood contribute to the progression of atherosclerosis, and if so, how?

Subsequent work has, of course, shown that atherosclerotic plaque formation may be exacerbated by immune cells with mutations associated with clonal hematopoiesis, thus raising the question of whether clonal enlargement in the blood should be targeted. therapeutically to prevent cardiovascular disease.

In a new study published in Cell, researchers at Massachusetts General Hospital and Harvard Medical School are now suggesting a different, additional possibility: Atherosclerosis causes clonal hematopoiesis. Patients with atherosclerosis suffer from hyperlipidemia and inflammation, two conditions known to cause a detrimental increase in hematopoietic gas cell division rates. In the new study, the researchers now show that this larger separation accelerates the development of clonal hematopoiesis.

Patients with atherosclerosis essentially experience an accelerated period of time. ‘This is because the rate at which genetic changes rise and spread through the hematopoietic system is determined by the basal level of gas cell division. “

Kamila Naxerova, PhD, Principal Author and Principal Investigator, Center for Systems Biology, Massachusetts General Hospital

“From a genetic point of view, you could say that atherosclerosis accelerates growth in the blood. Because clonal hematopoiesis is an age-related condition, atherosclerosis patients are more likely to develop earlier than healthy individuals,” he said. Naxerova, who is also an assistant professor of Radiation at Harvard Medical School.

Naxerova says her team ‘s findings may be good news for patients with clonal hematopoiesis: “There is no doubt that more research is needed to separate the link between clonal hematopoiesis and cardiovascular disease. But our results show that in some cases clonal hematopoiesis may be just a sign of relatively harmless overactive hematopoietic system, not a risk in itself. “

“What makes this study unique is that the interdisciplinary team applied mathematical modeling to find a new paradigm in the field of atherosclerosis and further clarified the interplay between cardiovascular disease. and clonal hematopoiesis, ”says Michelle Olive, PhD, Program Officer in the Department of Cardiovascular Sciences at the National Institute of Heart, Lung, and Blood, part of the National Institutes of Health.