Caveolin-1, cellular senescence and age-related diseases
Open accessAbstract
According to the "free radical theory" of aging, normal aging occurs as the result of tissue damages inflicted by reactive oxygen species (ROS) when ROS production exceeds the antioxidant capacity of the cell. ROS induce cellular dysfunctions such as stress-induced premature senescence (SIPS), which is believed to contribute to normal organismal aging and play a role in age-related diseases. Consistent with this hypothesis, increased oxidative damage of DNA, proteins, and lipids have been reported in aged animals and senescent cells accumulate in vivo with advancing age. Caveolin-1 acts as a scaffolding protein that concentrates and functionally regulates signaling molecules. Recently, great progress has been made toward understanding of the role of caveolin-1 in stress-induced premature senescence. Data show that caveolin-mediated signaling may contribute to explain, at the molecular level, how oxidative stress promotes the deleterious effects of cellular senescence such as aging and age-related diseases. In this review, we discuss the cellular mechanisms and functions of caveolin-1 in the context of SIPS and their relevance to the biology of aging.
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Senescent cells have an altered plasma membrane composition, with the most consistent change being upregulation of caveolin-1, an important component of cholesterol-enriched microdomains referred to as caveolae.
“Senescent cells also have an altered plasma membrane composition, with the most consistent change being upregulation of caveolin-1, an important component of cholesterol- enriched microdomains referred to as caveolae 60 .”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [60]
Section 4 (page unavailable) reports increased caveolin-1 expression in several types of senescent cells, and Section 1 identifies caveolin-1 as a structural component of cholesterol-enriched caveolae in the plasma membrane. The copy does not establish that caveolin-1 upregulation is the most consistent change in senescent cells’ plasma membrane composition. (LLM, conf=0.83)
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- Authors
- Zou, H., Stoppani, E., Volonte, D., & Galbiati, F.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Galbiati, Ferruccio
- Venue
- Mechanisms of Ageing and Development
- Publisher
- Elsevier BV
- Published
- 2011-11
- Volume
- 132
- Issue
- 11-12
- Pages
- 533-542
- ISSN
- 0047-6374 (ISSN-L)
- PMC
- PMC3243775
- OpenAlex
- W2051925288
- Cited by
- 112
- References
- 20
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 8 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 7 · 2019: 16 · 2018: 6 · 2017: 8 · 2016: 9 · 2015: 7 · 2014: 5 · 2013: 11 · 2012: 2
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Mechanisms of Ageing and Development (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- the National Institute on Aging (R01-AG030636)
- the Competitive Medical Research Fund of the UPMC Health System
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- caveolin-1, cellular senescence, stress-induced premature senescence, age-related diseases, free radical theory of aging, reactive oxygen species, oxidative stress, oxidative damage, senescent cells, aging
- MeSH terms
- Aging, Animals, Fibrosis, Humans, Infections, Models, Biological, Osteoarthritis, Pulmonary Emphysema, Wound Healing, Signal Transduction, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Cell Proliferation, Atherosclerosis, Caveolin 1, Intervertebral Disc Degeneration, Tumor Microenvironment
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