Cited by 232Nuclear Structure and FunctionTelomeres, Telomerase, and SenescenceHIV-related health complications and treatments

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

Caron, M, Auclair, M, Donadille, B, Béréziat, V, Guerci, B, Laville, M, Narbonne, H, Bodemer, C, Lascols, O, Capeau, J, Vigouroux, C·2007·Cell Death & Differentiation

DOI 10.1038/sj.cdd.4402197

Open this paper in CoChat — free account

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.

Integrity signals

Registry

Crossref · 10.1038/sj.cdd.4402197

Cites

45 of 45 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
A biomarker that identifies senescent human cells in culture and in aging skin in vivo.
Dimri, G. P., Lee, X., Basile, G., Acosta, M., Scott, G., Roskelley, C., Medrano, E. E., Linskens, M., Rubelj, I., & Pereira-Smith, O. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.20.9363 · Cited by 7,477
Mitochondria, Oxidants, and Aging
Balaban, R. S., Nemoto, S., & Finkel, T. (2005) · Cell · doi:10.1016/j.cell.2005.02.001 · Cited by 4,388
Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome
Eriksson, M., Brown, W. T., Gordon, L. B., Glynn, M. W., Singer, J., Scott, L., Erdos, M. R., Robbins, C. M., Moses, T. Y., Berglund, P., et al. (2003) · Nature · doi:10.1038/nature01629 · Cited by 1,990
Lamin a truncation in Hutchinson-Gilford progeria
De Sandre-Giovannoli, A., Bernard, R., Cau, P., Navarro, C., Amiel, J., Boccaccio, I., Lyonnet, S., Stewart, C. L., Munnich, A., Le Merrer, M., et al. (2003) · Science · doi:10.1126/science.1084125 · Cited by 1,346
Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson–Gilford progeria syndrome
Goldman, R. D., Shumaker, D. K., Erdos, M. R., Eriksson, M., Goldman, A. E., Gordon, L. B., Gruenbaum, Y., Khuon, S., Mendez, M., Varga, R., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0402943101 · Cited by 1,103
Cardiovascular Risk and Body-Fat Abnormalities in HIV-Infected Adults
Grinspoon, S. K., & Carr, A. D. (2005) · New England Journal of Medicine · doi:10.1056/nejmra041811 · Cited by 1,073
The signals and pathways activating cellular senescence
Ben-Porath, I., & Weinberg, R. A. (2005) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2004.10.013 · Cited by 1,046
Mitochondrial toxicity induced by nucleoside-analogue reverse-transcriptase inhibitors is a key factor in the pathogenesis of antiretroviral-therapy-related lipodystrophy
Brinkman, K., Smeitink, J. A. M., Romijn, J. A., & Reiss, P. (1999) · The Lancet · doi:10.1016/s0140-6736(99)06102-4 · Cited by 863
Genomic instability in laminopathy-based premature aging
Liu, B., Wang, J., Chan, K. M., Tjia, W. M., Deng, W., Guan, X., Huang, J.-D., Li, K. M., Chau, P. Y., Chen, D. J., et al. (2005) · Nature Medicine · doi:10.1038/nm1266 · Cited by 650
Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation
Varela, I., Cadiñanos, J., Pendás, A. M., Gutiérrez-Fernández, A., Folgueras, A. R., Sánchez, L. M., Zhou, Z., Rodríguez, F. J., Stewart, C. L., Vega, J. A., et al. (2005) · Nature · doi:10.1038/nature04019 · Cited by 466
Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect
Bergö, M. O., Gavino, B. J., Ross, J., Schmidt, W. K., Hong, C., Kendall, L. V., Mohr, A., Meta, M. D., Genant, H. K., Jiang, Y., et al. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.192460799 · Cited by 443
LMNA mutations in atypical Werner's syndrome
Chen, L., Lee, L., Kudlow, B. A., dos Santos, H. G., Sletvold, O., Shafeghati, Y., Botha, E. G., Garg, A., Hanson, N. B., Martin, G. M., et al. (2003) · The Lancet · doi:10.1016/s0140-6736(03)14069-x · Cited by 433
Association between altered expression of adipogenic factor SREBP1 in lipoatrophic adipose tissue from HIV-1-infected patients and abnormal adipocyte differentiation and insulin resistance
Bastard, J., Caron, M., Vidal, H., Jan, V., Auclair, M., Vigouroux, C., Luboinski, J., Laville, M., Maachi, M., Girard, P., et al. (2002) · The Lancet · doi:10.1016/s0140-6736(02)08094-7 · Cited by 405
Self-citation
Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome
Capell, B. C., Erdos, M. R., Madigan, J. P., Fiordalisi, J. J., Varga, R., Conneely, K. N., Gordon, L. B., Der, C. J., Cox, A. D., & Collins, F. S. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506001102 · Cited by 395
A Protein Farnesyltransferase Inhibitor Ameliorates Disease in a Mouse Model of Progeria
Fong, L. G., Frost, D. J., Meta, M. D., Qiao, X., Yang, S. H., Coffinier, C., & Young, S. G. (2006) · Science · doi:10.1126/science.1124875 · Cited by 315
Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson–Gilford progeria syndrome mutation
Yang, S. H., Bergö, M. O., Toth, J. I., Qiao, X., Hu, Y., Sandoval, S., Meta, M. D., Bendale, P. M., Gelb, M. H., Young, S. G., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0504641102 · Cited by 311
The HIV Protease Inhibitor Indinavir Impairs Sterol Regulatory Element-Binding Protein-1 Intranuclear Localization, Inhibits Preadipocyte Differentiation, and Induces Insulin Resistance
Caron, M., Auclair, M., Vigouroux, C., Glorian, M., Forest, C. D., & Capeau, J. (2001) · Diabetes · doi:10.2337/diabetes.50.6.1378 · Cited by 308
Self-citation
Oxidants and aging
Beckman, K. B., & Ames, B. N. (2000) · Elsevier eBooks · doi:10.1016/b978-044482650-3/50027-4 · Cited by 307
Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors
Navarro, C. L., Cadiñanos, J., Sandre‐Giovannoli, A. D., Bernard, R., Courrier, S., Boccaccio, I., Boyer, A., Kleijer, W. J., Wagner, A., Giuliano, F., et al. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi159 · Cited by 299
Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes
Toth, J. I., Yang, S. H., Qiao, X., Beigneux, A. P., Gelb, M. H., Moulson, C. L., Miner, J. H., Young, S. G., & Fong, L. G. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0505767102 · Cited by 292
Accumulation of Short Telomeres in Human Fibroblasts Prior to Replicative Senescence
Martens, U. M., Chavez, E. A., Poon, S. S. S., Schmoor, C., & Lansdorp, P. M. (2000) · Experimental Cell Research · doi:10.1006/excr.2000.4823 · Cited by 263
Incomplete processing of mutant lamin A in Hutchinson–Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition
Glynn, M. W., & Glover, T. W. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi326 · Cited by 259
Prelamin A and lamin A appear to be dispensable in the nuclear lamina
Fong, L. G. (2006) · Journal of Clinical Investigation · doi:10.1172/jci27125 · Cited by 249
Nuclear envelope disorganization in fibroblasts from lipodystrophic patients with heterozygous R482Q/W mutations in the lamin A/C gene
Vigouroux, C., Auclair, M., Dubosclard, E., Pouchelet, M., Capeau, J., Courvalin, J., & Buendia, B. (2001) · Journal of Cell Science · doi:10.1242/jcs.114.24.4459 · Cited by 239
Self-citation
Altered pre-lamin A processing is a common mechanism leading to lipodystrophy
Capanni, C., Mattioli, E., Columbaro, M., Lucarelli, E., Parnaik, V. K., Novelli, G., Wehnert, M. S., Cenni, V., Maraldi, N. M., Squarzoni, S., et al. (2005) · Human Molecular Genetics · doi:10.1093/hmg/ddi158 · Cited by 226
Thematic Review Series: Lipid Posttranslational Modifications. Prelamin A, Zmpste24, misshapen cell nuclei, and progeria—new evidence suggesting that protein farnesylation could be important for disease pathogenesis
Young, S. G., Fong, L. G., & Michaelis, S. (2005) · Journal of Lipid Research · doi:10.1194/jlr.r500011-jlr200 · Cited by 218
Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24 -deficient mice
Fong, L. G., Ng, J. K., Meta, M. D., Coté, N., Yang, S. H., Stewart, C. L., Sullivan, T., Burghardt, A. J., Majumdar, S., Reue, K., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0408558102 · Cited by 209
A New Clinical Condition Linked to a Novel Mutation in Lamins A and C with Generalized Lipoatrophy, Insulin-Resistant Diabetes, Disseminated Leukomelanodermic Papules, Liver Steatosis, and Cardiomyopathy
Caux, F. A., Dubosclard, E., Lascols, O., Buendia, B., Chazouillères, O., Cohen, A. A., Courvalin, J., Laroche, L., Capeau, J., Vigouroux, C., et al. (2003) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2002-021506 · Cited by 196
Self-citation
Lamin A/C gene: sex-determined expression of mutations in Dunnigan-type familial partial lipodystrophy and absence of coding mutations in congenital and acquired generalized lipoatrophy.
Vigouroux, C., Magré, J., Vantyghem, M., Bourut, C., Lascols, O., Shackleton, S., Lloyd, D. J., Guerci, B., Padova, G., Valensi, P. E., et al. (2000) · Diabetes · doi:10.2337/diabetes.49.11.1958 · Cited by 179
Self-citation
Some HIV protease inhibitors alter lamin A/C maturation and stability, SREBP-1 nuclear localization and adipocyte differentiation
Caron, M., Auclair, M., Sterlingot, H., Kornprobst, M., & Capeau, J. (2003) · AIDS · doi:10.1097/00002030-200311210-00005 · Cited by 176
Self-citation
Nuclear lamins, diseases and aging
Mattout, A., Dechat, T., Adam, S. A., Goldman, R. D., & Gruenbaum, Y. (2006) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2006.03.007 · Cited by 171
Altered Fat Differentiation and Adipocytokine Expression are Inter-Related and Linked to Morphological Changes and Insulin Resistance in HIV-1-Infected Lipodystrophic Patients
Jan, V., Cervera, P., Maachi, M., Baudrimont, M., Kim, M. J., Vidal, H., Girard, P., Levan, P., Rozenbaum, W., Lombès, A., et al. (2004) · Antiviral Therapy · doi:10.1177/135965350400900412 · Cited by 169
Self-citation
Effects of atazanavir/ritonavir and lopinavir/ritonavir on glucose uptake and insulin sensitivity: demonstrable differences in vitro and clinically
Noor, M. A., Flint, O. P., Maa, J., & Parker, R. A. (2006) · AIDS · doi:10.1097/01.aids.0000244200.11006.55 · Cited by 155
Mitochondrial DNA and aging
ALEXEYEV, M. F., LeDoux, S. P., & Wilson, G. L. (2004) · Clinical Science · doi:10.1042/cs20040148 · Cited by 151
Loss of Proliferative Capacity and Induction of Senescence in Oxidatively Stressed Human Fibroblasts
Chen, J., Stoeber, K., Kingsbury, S. R., Ozanne, S. E., Williams, G. H., & Hales, C. N. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m409153200 · Cited by 148
Nuclear lamin A inhibits adipocyte differentiation: implications for Dunnigan-type familial partial lipodystrophy
Boguslavsky, R. L., Stewart, C. L., & Worman, H. J. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddi480 · Cited by 146
Comparison of potential markers of farnesyltransferase inhibition.
Adjei, A. A., Davis, J. N., Erlichman, C., Svingen, P. A., & Kaufmann, S. H. (2000) · PubMed · Cited by 119
The HIV-1 nucleoside reverse transcriptase inhibitors stavudine and zidovudine alter adipocyte functions in vitro
Caron, M., Auclair, M., Lagathu, C., Lombès, A., Walker, U. A., Kornprobst, M., & Capeau, J. (2004) · AIDS · doi:10.1097/00002030-200411050-00004 · Cited by 107
Self-citation
Understanding aging: revealing order out of chaos
Dufour, É., & Larsson, N. (2004) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2004.04.020 · Cited by 103
LIPOFUSCIN ACCUMULATION AND AGEING OF FIBROBLASTS
von Zglinicki, T., Nilsson, E., Döcke, W. D., & Brunk, U. T. (2009) · Gerontology · doi:10.1159/000213728 · Cited by 85
Contribution of p16INK4a to replicative senescence of human fibroblasts
Brookes, S., Rowe, J., del Arroyo, A. G., BOND, J. A., & Peters, G. G. (2004) · Experimental Cell Research · doi:10.1016/j.yexcr.2004.04.035 · Cited by 85
The Free Radical Theory of Aging: The Effect of Age on Serum Mercaptan Levels
Harman, D. (1960) · Journal of Gerontology · doi:10.1093/geronj/15.1.38 · Cited by 73
HIV protease inhibitors block adipocyte differentiation independently of lamin A/C
Kudlow, B. A., Jameson, S. A., & Kennedy, B. K. (2005) · AIDS · doi:10.1097/01.aids.0000186827.91408.90 · Cited by 33
Growing old with HIV
Senior, K. (2005) · The Lancet Infectious Diseases · doi:10.1016/s1473-3099(05)70279-6 · Cited by 13

Flagged first, then by citations

Sorted by citations

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
Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin
Dechat, T., Pfleghaar, K., Sengupta, K., Shimi, T., Shumaker, D. K., Solimando, L., & Goldman, R. D. (2008) · Genes & Development · doi:10.1101/gad.1652708 · Cited by 940
Lipodystrophies: Genetic and Acquired Body Fat Disorders
Garg, A. (2011) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-1159 · Cited by 556
“Adipocyte loss in patients with LMNA mutations may be due to disruption of nuclear envelope functionand integrity resulting in premature cell death (63).”
Background
Mechanics 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

See all 232

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
ORCID: Auclair, M
Donadille, B
Béréziat, V
Guerci, B
Laville, M
Bodemer, C
Capeau, J
Vigouroux, C
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2007-07-06
Volume: 14
Issue: 10
Pages: 1759-1767
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/sj.cdd.4402197
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

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

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

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks