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DNA damage as a new emerging risk factor in atherosclerosis
Maria Grazia Andreassi1, Nicoletta Botto
1Laboratory of Cellular Biology, CNR Institute of Clinical Physiology, G. Pasquinucci Hospital, Via Aurelia Sud-Montepepe, 54100 Massa, Italy. andreas@ifc.cnr.it
Trends in Cardiovascular Medicine
|October 3, 2003
Summary
Genetic alterations and DNA damage are implicated in atherosclerosis, a chronic inflammatory disease. Studying these somatic cell changes may reveal new insights into disease mechanisms and novel therapeutic strategies.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Genetics
Background:
- Atherosclerosis is a leading cause of mortality in Western societies.
- It involves a chronic fibroproliferative-inflammatory response of the arterial intima, forming atherosclerotic plaques.
- Similarities exist between atherosclerotic and carcinogenic processes, suggesting a potential
- mutation theory of atherosclerosis.
Purpose of the Study:
- To review studies supporting the role of genetic alterations in atherosclerosis.
- To explore the link between DNA damage and atherogenesis.
- To highlight potential novel therapeutic approaches based on DNA damage research.
Main Methods:
- Review of experimental evidence and published studies.
- Analysis of genomic alterations in smooth muscle cells of human plaques.
- Assessment of biomarkers of carcinogenic exposure, including DNA adducts and cytogenetic endpoints.
Main Results:
- Microsatellite instability and loss of heterozygosity observed in human plaque smooth muscle cells.
- Genomic destabilization suggested as a pivotal mechanism in atherosclerosis.
- Evidence indicates somatic cell alterations are critical in the atherogenic process.
Conclusions:
- Genetic alterations and DNA damage play a significant role in the pathogenesis of atherosclerosis.
- Further study of DNA damage may provide novel insights into disease mechanisms.
- This research could lead to the development of new therapeutic strategies for atherosclerosis.