ArticleOncotarget2015
All-trans retinoic acid and rapamycin normalize Hutchinson Gilford progeria fibroblast phenotype.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 80 citations in OpenAlex.
- Selection of specific and efficient siRNAs in new cellular model for Hutchinson-Gilford progeria syndrome therapy.Molecular therapy. Nucleic acids · 2025Article
- From Genome to Geroscience: How DNA Damage Shapes Systemic Decline.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Involvement of NRF2 and AMPK signaling in aging and progeria: a digest.Redox biology · 2025Review
- Recurrent somatic mutation and progerin expression in early vascular aging of chronic kidney disease.Nature aging · 2025Article
- Decreasing Lamin A Triggers Cell Fate Transitions through Heterochromatin-Nuclear Periphery Detethering.Biomaterials research · 2025Article
- A multiparametric screen uncovers FDA-approved small molecules that potentiate the nuclear mechano-dysfunctions in ATR-defective cells.Scientific reports · 2024Article
- Senescence, regulators of alternative splicing and effects of trametinib treatment in progeroid syndromes.GeroScience · 2024Article
- Review
- Nuclear envelope morphology change upon repetitive treatment with modified antisense oligonucleotides targeting Hutchinson-Gilford Progeria Syndrome.Biochemistry and biophysics reports · 2023Article
- Filamentous nuclear actin regulation of PML NBs during the DNA damage response is deregulated by prelamin A.Cell death & disease · 2022Article
- Quality control mechanisms that protect nuclear envelope identity and function.The Journal of cell biology · 2022Review
- Review
- The role of prelamin A post-translational maturation in stress response and 53BP1 recruitment.Frontiers in cell and developmental biology · 2022Article
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- Lamin regulates the dietary restriction response via the mTOR pathway in Caenorhabditis elegans.Journal of cell science · 2021Article
- Small-Molecule Therapeutic Perspectives for the Treatment of Progeria.International journal of molecular sciences · 2021Review
- The progeria research foundation 10Aging · 2021Article
- Systematic screening identifies therapeutic antisense oligonucleotides for Hutchinson-Gilford progeria syndrome.Nature medicine · 2021Article
- From structural resilience to cell specification - Intermediate filaments as regulators of cell fate.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson Gilford progeria syndrome is a fatal disorder characterized by accelerated aging, bone resorption and atherosclerosis, caused by a LMNA mutation which produces progerin, a mutant lamin A precursor. Progeria cells display progerin and prelamin A nuclear accumulation, altered histone methylation pattern, heterochromatin loss, increased DNA damage and cell cycle alterations. Since the LMNA promoter contains a retinoic acid responsive element, we investigated if all-trans retinoic acid administration could lower progerin levels in cultured fibroblasts. We also evaluated the effect of associating rapamycin, which induces autophagic degradation of progerin and prelamin A. We demonstrate that all-trans retinoic acid acts synergistically with low-dosage rapamycin reducing progerin and prelamin A, via transcriptional downregulation associated with protein degradation, and increasing the lamin A to progerin ratio. These effects rescue cell dynamics and cellular proliferation through recovery of DNA damage response factor PARP1 and chromatin-associated nuclear envelope proteins LAP2α and BAF. The combined all-trans retinoic acid-rapamycin treatment is dramatically efficient, highly reproducible, represents a promising new approach in Hutchinson-Gilford Progeria therapy and deserves investigation in ageing-associated disorders.
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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.