Mechanisms of cardiovascular disease in accelerated aging syndromes.
In the past several years, remarkable progress has been made in the understanding of the mechanisms of premature aging. These rare, genetic conditions offer valuable insights into the normal aging process and the complex biology of cardiovascular disease. Many of these advances have been made in the most dramatic of these disorders, Hutchinson-Gilford progeria syndrome. Although characterized by features of normal aging such as alopecia, skin wrinkling, and osteoporosis, patients with Hutchinson-Gilford progeria syndrome are affected by accelerated, premature arteriosclerotic disease that leads to heart attacks and strokes at a mean age of 13 years. In this review, we highlight recent advances in the biology of premature aging uncovered in Hutchinson-Gilford progeria syndrome and other accelerated aging syndromes, advances that provide insight into the mechanisms of cardiovascular diseases ranging from atherosclerosis to arrhythmias.
Capell
Brian C
BC
Genome Technology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892-2486, USA.
Collins
Francis S
FS
Nabel
Elizabeth G
EG
D019588:Aging, Premature / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D002318:Cardiovascular Diseases / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology*; D006801:Humans; D011371:Progeria / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology*; D013577:Syndrome; D014898:Werner Syndrome / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology*