Key result
Baseline DNA damage and mutagen sensitivity were significantly elevated in peripheral blood mononuclear cells from patients with pulmonary arterial hypertension and their unaffected relatives compared to controls.
Why the study?
Are DNA damage, mutagen sensitivity, and reactive oxygen species levels intrinsically higher in patients with PAH and their unaffected relatives compared to controls?
Population
Patients with Group 1 pulmonary arterial hypertension, their unaffected relatives, and unrelated control…
Design
Case-control
Authors
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Supports heritable predisposition in PAH families; leaves open whether targeting DNA damage or ROS alters progression.
Case-Control
No
Are DNA damage, mutagen sensitivity, and reactive oxygen species levels intrinsically higher in patients with PAH and their unaffected relatives compared to controls?
p-value: p=<0.001
Increased baseline and mutagen-induced DNA damage in PAH cells and unaffected relatives suggests a genetically determined trait that predates disease onset and may contribute to vascular remodeling.
Federici et al. (2015) conducted a case-control in Pulmonary Arterial Hypertension. Pulmonary arterial hypertension and genetic susceptibility vs. Unrelated healthy control subjects was evaluated on Baseline DNA damage in peripheral blood mononuclear cells (PBMC) (p=<0.001). Baseline DNA damage and mutagen sensitivity were significantly elevated in peripheral blood mononuclear cells from patients with pulmonary arterial hypertension and their unaffected relatives compared to controls.
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