Key result
Arteriosclerotic plaque DNA induces tumors in mice, suggesting somatic cell alterations drive plaque development.
Why the study?
The specific contributions of environmental and genetic factors to the onset and development of cardiovascular disease remain unclear.
Population
Animal models and human arteriosclerotic plaque DNA
Comparison
Environmental agents (chemical mutagens, viruses) and plaque DNA effects
Design
Preclinical studies including in vitro and animal model experiments
Authors
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Extends monoclonal hypothesis in animal models; leaves open whether somatic mutations drive human plaque formation.
This study provides preclinical evidence supporting the monoclonal hypothesis that somatic cell alterations, potentially driven by environmental agents, play a critical role in the development of arteriosclerotic plaques.
Arthur Penn (1989) conducted a review in Cardiovascular disease / arteriosclerotic plaques. Environmental agents (chemical mutagens, viruses) was evaluated. DNA from human arteriosclerotic plaques transforms cells in vitro and induces tumor formation in nude mice, suggesting somatic cell alterations are critical to plaque development.
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