The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence
Abstract
Lipodystrophic syndromes associated with mutations in LMNA, encoding A-type lamins, and with HIV antiretroviral treatments share several clinical characteristics. Nuclear alterations and prelamin A accumulation have been reported in fibroblasts from patients with LMNA mutations and adipocytes exposed to protease inhibitors (PI). As genetically altered lamin A maturation also results in premature ageing syndromes with lipodystrophy, we studied prelamin A expression and senescence markers in cultured human fibroblasts bearing six different LMNA mutations or treated with PIs. As compared to control cells, fibroblasts with LMNA mutations or treated with PIs had nuclear shape abnormalities and reduced proliferative activity that worsened with increasing cellular passages. They exhibited prelamin A accumulation, increased oxidative stress, decreased expression of mitochondrial respiratory chain proteins and premature cellular senescence. Inhibition of prelamin A farnesylation prevented cellular senescence and oxidative stress. Adipose tissue samples from patients with LMNA mutations or treated with PIs also showed retention of prelamin A, overexpression of the cell cycle checkpoint inhibitor p16 and altered mitochondrial markers. Thus, both LMNA mutations and PI treatment result in accumulation of farnesylated prelamin A and oxidative stress that trigger premature cellular senescence. These alterations could participate in the pathophysiology of lipodystrophic syndromes and lead to premature ageing complications.
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“To our knowledge, no evidence yet exists on whether antiretroviral compounds can induce senescence in adipocytes in vitro, but it has been demonstrated that protease inhibitors and NRTIs can induce p16 and p21 expression in human adipose tissue (Caron et al, 2007, 2008).”
From The struggle of a good friend getting old: cellular senescence in viral responses and therapy (2021) · cites this paper as Caron et al, 2007
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Cellular senescence and senolytics: the path to the clinic
Chaib, S., Tchkonia, T., & Kirkland, J. L. (2022) · Nature Medicine · doi:10.1038/s41591-022-01923-y · Cited by 1,134
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Lipodystrophies: Genetic and Acquired Body Fat Disorders
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“Adipocyte loss in patients with LMNA mutations may be due to disruption of nuclear envelope functionand integrity resulting in premature cell death (63).”
BackgroundMechanics and functional consequences of nuclear deformations
Kalukula, Y., Stephens, A. D., Lammerding, J., & Gabriele, S. (2022) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-022-00480-z · Cited by 475
Energetics, epigenetics, mitochondrial genetics
Wallace, D. C., & Fan, W. (2009) · Mitochondrion · doi:10.1016/j.mito.2009.09.006 · Cited by 519
Metadata
- Authors
- Caron, M., Auclair, M., Donadille, B., Béréziat, V, Guerci, B., Laville, M., Narbonne, H., Bodemer, C., Lascols, O., Capeau, J., & Vigouroux, C.
- Affiliations
- Inserm (FR)
- Centre Hospitalier Régional et Universitaire de Nancy (FR)
- Hospices Civils de Lyon (FR)
- Assistance Publique Hôpitaux de Marseille (FR)
- Hôpital Necker-Enfants Malades (FR)
- Corresponding author
- Caron, M
- Venue
- Cell Death & Differentiation
- Published
- 2007-07-06
- Volume
- 14
- Issue
- 10
- Pages
- 1759-1767
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- OpenAlex
- W1979927283
- Cited by
- 226
- References
- 45
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 12 · 2021: 33 · 2020: 8 · 2019: 7 · 2018: 7 · 2017: 9 · 2016: 15 · 2015: 9 · 2014: 12 · 2013: 17 · 2012: 10
- FWCI
- 6.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell Death and Differentiation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Styrelsen för Internationellt Utvecklingssamarbete
- Sidaction
- European Commission
- Institut National de la Santé et de la Recherche Médicale
- Servier
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Infectious Diseases › HIV-related health complications and treatments
- Keywords
- lipodystrophy, LMNA mutations, A-type lamins, HIV protease inhibitors, oxidative stress, premature aging, farnesylation, p16, mitochondrial respiratory chain, nuclear abnormalities, fibroblasts, adipose tissue
- MeSH terms
- Adult, Biopsy, Cells, Cultured, Child, Female, Fibroblasts, Humans, Middle Aged, Mitochondria, Mutation, Nuclear Proteins, Protein Precursors, Cellular Senescence, HIV Protease Inhibitors, Reactive Oxygen Species, Oxidative Stress, Indinavir, Nelfinavir, Cyclin-Dependent Kinase Inhibitor p16, Lamin Type A, Cyclin-Dependent Kinase Inhibitor p21, Lipodystrophy, Familial Partial, Cell Nucleus Shape
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