Sleep and exercise affected inflammation linked to certain blood-cell mutations in a study combining human data and mouse experiments. The findings, published in Nature on June 10, 2026, do not establish that changing these habits prevents heart attacks in people with those mutations.
The researchers examined clonal hematopoiesis, in which blood cells carrying particular mutations expand. Such changes can contribute to inflammation and plaque buildup inside arteries.
The mutation made a difference
Human datasets linked greater physical activity with a lower prevalence of clonal hematopoiesis involving mutations other than DNMT3A. This was an association, not a clinical trial proving prevention.
In mice, uninterrupted sleep or exercise limited expansion of cells with Jak2 or Tet2 mutations. That response was absent in the Trp53 and Dnmt3a models tested.
Artery plaque was a separate outcome: sleep or exercise reduced atherosclerosis in the Jak2, Tet2 and Trp53 models, but not the Dnmt3a model. In the Jak2 experiments, exercise activated neurons in the locus coeruleus, with noradrenaline signalling helping suppress inflammation.
What the study cannot tell readers
A result involving mutant cells or artery plaque is not the same as a demonstrated reduction in heart attacks. Readers should distinguish the human association from the mechanisms tested in animals; neither establishes a personalised treatment plan.
Source: Original research in Nature.
Correction, October 19, 2026: We removed contradictory passages and an unsupported graphic, corrected scientific names, and clarified the limits of the evidence.