Mechanisms of cardiovascular disease in accelerated aging syndromes
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.”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [126]
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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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