ArticleAging2014
Prelamin A accumulation and stress conditions induce impaired Oct-1 activity and autophagy in prematurely aged human mesenchymal stem cell.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed.
- Crosstalk between lipid metabolism and epigenetics in cellular senescence and age-related diseases.npj aging · 2026Review
- Article
- "Bone-SASP" in Skeletal Aging.Calcified tissue international · 2023Review
- Lamin A to Z in normal aging.Aging · 2022Article
- Cellular Metabolism and Bioenergetic Function in Human Fibroblasts and Preadipocytes of Type 2 Familial Partial Lipodystrophy.International journal of molecular sciences · 2022Article
- Cell and Cell-Free Therapies to Counteract Human Premature and Physiological Aging: MSCs Come to Light.Journal of personalized medicine · 2021Review
- From Stem Cells to Bone-Forming Cells.International journal of molecular sciences · 2021Review
- Apelin Rejuvenates Aged Human Mesenchymal Stem Cells by Regulating Autophagy and Improves Cardiac Protection After Infarction.Frontiers in cell and developmental biology · 2021Article
- The emerging role of cellular senescence in complications of COVID-19.Cancer treatment and research communications · 2021Review
- Review
- Review
- Vitamin C Treatment Rescues Prelamin A-Induced Premature Senescence of Subchondral Bone Mesenchymal Stem Cells.Stem cells international · 2020Article
- Dual Role of Autophagy in Regulation of Mesenchymal Stem Cell Senescence.Frontiers in cell and developmental biology · 2020Review
- Mesenchymal Stem Cell Senescence and Rejuvenation: Current Status and Challenges.Frontiers in cell and developmental biology · 2020Review
- Altered adipocyte differentiation and unbalanced autophagy in type 2 Familial Partial Lipodystrophy: an in vitro and in vivo study of adipose tissue browning.Experimental & molecular medicine · 2019Article
- The Cutting Edge: The Role of mTOR Signaling in Laminopathies.International journal of molecular sciences · 2019Review
- Ankrd2 in Mechanotransduction and Oxidative Stress Response in Skeletal Muscle: New Cues for the Pathogenesis of Muscular Laminopathies.Oxidative medicine and cellular longevity · 2019Review
- Nuclear Nox4 interaction with prelamin A is associated with nuclear redox control of stem cell aging.Aging · 2018Article
- Osteogenesis and aging: lessons from mesenchymal stem cells.Stem cell research & therapy · 2018Review
- GATA4-dependent regulation of the secretory phenotype via MCP-1 underlies lamin A-mediated human mesenchymal stem cell aging.Experimental & molecular medicine · 2018Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging, a time-dependent functional decline of biological processes, is the primary risk factor in developing diseases such as cancer, cardiovascular or degenerative diseases. There is a real need to understand the human aging process in order to increase the length of disease-free life, also known as "health span". Accumulation of progerin and prelamin A are the hallmark of a group of premature aging diseases but have also been found during normal cellular aging strongly suggesting similar mechanisms between healthy aging and LMNA-linked progeroid syndromes. How this toxic accumulation contributes to aging (physiological or pathological) remains unclear. Since affected tissues in age-associated disorders and in pathological aging are mainly of mesenchymal origin we propose a model of human aging based on mesenchymal stem cells (hMSCs) which accumulate prelamin A. We demonstrate that prelamin A-accumulating hMSCs have a premature aging phenotype which affects their functional competence in vivo. The combination of prelamin A accumulation and stress conditions enhance the aging phenotype by dysregulating the activity of the octamer binding protein Oct-1This experimental model has been fundamental to identify a new role for Oct-1 in hMSCs aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.