Scientists have uncovered the mechanism by which senescent cells turn into a heart attack trigger

Researchers have discovered a molecular mechanism by which aging vascular cells destabilize atherosclerotic plaques and provoke the formation of blood clots. This was reported on June 4 in the journal Medical Xpress.

The object of the study was senescent cells — stressed and senescent cells that stop dividing but do not die. Scientists have found that the loss of key regulatory proteins LATS1/2 in such cells activates the CD38 enzyme. It reprograms energy metabolism, makes cells unstable, and triggers inflammation inside plaques, leading to atherothrombosis, the formation of blood clots that can cause a heart attack or stroke.

The experiments were conducted on preclinical models using advanced molecular profiling. Removal of LATS1/2 in the endothelial cells lining the inner surface of the vessels transformed them into a senescent but abnormally active state. The result was instability and increased vascular permeability, inflammation, abnormal growth of new vessels and the formation of prothrombotic plaques.

Subsequent analysis revealed a sharp increase in CD38 levels in the senescent cells. Overexpression of this enzyme rearranged the metabolism of the endothelium: cells consumed excess energy, which accelerated inflammation and destabilized plaques. Blocking CD38 reversed these effects, both in cell culture and in a living organism. The data obtained were verified on plaque samples from patients who demonstrated the same metabolic signatures and molecular pathways.

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On March 23, Medical Xpress reported on the impact of lifestyle on heart health. According to the publication, the combination of even minor improvements in sleep patterns, nutrition, and physical activity levels can significantly reduce the likelihood of stroke, heart attack, and heart failure.