Loss of a DNA regulator speeds lung vessel aging in mice
Mice lacking the regulator developed high lung blood pressure by 8 months; right-heart pumping pressure exceeded 40 millimeters of mercury, compared with control mice.
Our read
Mechanisms- Studied:
- Experiments in endothelial cell-specific Tet2 knockout mice, 8 months, against littermate controls
- What changed:
- RVSP exceeded 40 mmHg in Tet2 knockout mice compared with controls
- The catch:
- Barrier impairment was inferred from a protein measurement
- Why it’s aging research:
- It studies something that builds up in the body with age.
Editor of record: Boris Djordjevic · AgingResearch.News
Mice engineered to lose Tet2 in endothelial cells, which line blood vessels, developed pulmonary hypertension—high pressure in lung blood vessels—by 8 months in an animal experiment. Researchers compared them with littermate controls. TET2 is a protein that regulates chemical marks on DNA.
The altered mice had pressure exceeding 40 millimeters of mercury in the heart’s right lower chamber during contraction. Their lungs showed abnormal remodeling of small blood vessels, scarring and premature endothelial senescence, a state in which cells stop dividing. Levels of VE-cadherin, a protein that helps cells stay joined, fell, suggesting a weakened vessel barrier. Cell tracking also revealed abnormal changes in capillary lining cells. The authors suggested that loss of these cells’ identity links vascular aging to pulmonary vascular disease.
Why it matters
Aging in blood vessel lining cells may contribute to pulmonary hypertension, whose burden rises with age. The findings provide a mouse model for investigating that link.
Caveats
Barrier impairment was inferred from a protein measurement. The conference abstract does not give group sizes, and the findings concern genetically altered mice, not people.
The paper
Univ of Illinois at Chicago; Univ of Illinois Chicago
AHA Scientific Sessions 2026 Abstract, Nov 2, 2026
Presented at AHA Scientific Sessions 2026, abstract 10646
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