Cited by 134Nuclear Structure and FunctionTelomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model Organisms

Mechanisms of cardiovascular disease in accelerated aging syndromes

Capell, Brian C., Collins, Francis S., Nabel, Elizabeth G.·2007·Circulation Research

Abstract

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.

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  • The capability of cellular senescence to drive atherosclerosis independently of chronological ageing and classical risk factor exposure is seen in human progeria syndromes.

    “In clinical practice, the capability of cellular senescence to drive atherosclerosis independently of chronological ageing and classical risk factor exposure is seen in drastic examples of human progeria syndromes, such as Hutchinson–Gilford progeria (HGS), Werner syndrome, and other laminopathies.”

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References 149 · Cited by 134

Authors
Capell, B. C., Collins, F. S., & Nabel, E. G.
Affiliations
National Institutes of Health (US)
Venue
Circulation Research
Published
2007-07-06
Volume
101
Issue
1
Pages
13-26
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2127608128
Cited by
134
References
149
Citations by year
2026: 3 · 2025: 3 · 2024: 3 · 2023: 5 · 2022: 5 · 2021: 5 · 2020: 4 · 2019: 6 · 2018: 4 · 2017: 8 · 2016: 11 · 2015: 7 · 2014: 14 · 2013: 13 · 2012: 14
FWCI
0.44
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
premature aging, Hutchinson-Gilford progeria syndrome, cardiovascular disease, atherosclerosis, cardiac arrhythmias
MeSH terms
Animals, Cardiovascular Diseases, Humans, Progeria, Syndrome, Werner Syndrome, Aging, Premature

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