ArticleOncotarget2016
Vitamin D receptor signaling improves Hutchinson-Gilford progeria syndrome cellular phenotypes.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- A toxic STING-SAMHD1 axis drives replication stress in progeria and cancer cells.Nucleic acids research · 2026Article
- Vitamin D receptor signaling in inflammatory senescence-associated skin aging: Mechanisms and therapeutic potentials.Journal of cell communication and signaling · 2026Article
- STING causes replication stress and nascent DNA degradation via SAMHD1.bioRxiv : the preprint server for biology · 2026Article
- Vitamin D and Brain Health.Advances in experimental medicine and biology · 2026Review
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- Involvement of NRF2 and AMPK signaling in aging and progeria: a digest.Redox biology · 2025Review
- A noncanonical cGAS-STING pathway drives cellular and organismal aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A hypothesis: MiRNA-124 mediated regulation of sirtuin 1 and vitamin D receptor gene expression accelerates aging.Aging medicine (Milton (N.S.W)) · 2024Article
- STAT1 Drives the Interferon-Like Response and Aging Hallmarks in Progeria.Aging biology · 2023Article
- Loss of FAM111B protease mutated in hereditary fibrosing poikiloderma negatively regulates telomere length.Frontiers in cell and developmental biology · 2023Article
- Review
- Gene-Regulatory Potential of 25-Hydroxyvitamin DFrontiers in nutrition · 2022Article
- The role of prelamin A post-translational maturation in stress response and 53BP1 recruitment.Frontiers in cell and developmental biology · 2022Article
- Transcriptome-Wide Profile of 25-Hydroxyvitamin DNutrients · 2021Article
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- Hydrogen sulfide in ageing, longevity and disease.The Biochemical journal · 2021Review
- Systematic screening identifies therapeutic antisense oligonucleotides for Hutchinson-Gilford progeria syndrome.Nature medicine · 2021Article
- Article
- Progress and trends in the development of therapies for Hutchinson-Gilford progeria syndrome.Aging cell · 2020Review
- Genome-Protecting Compounds as Potential Geroprotectors.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is a devastating incurable premature aging disease caused by accumulation of progerin, a toxic lamin A mutant protein. HGPS patient-derived cells exhibit nuclear morphological abnormalities, altered signaling pathways, genomic instability, and premature senescence. Here we uncover new molecular mechanisms contributing to cellular decline in progeria. We demonstrate that HGPS cells reduce expression of vitamin D receptor (VDR) and DNA repair factors BRCA1 and 53BP1 with progerin accumulation, and that reconstituting VDR signaling via 1α,25-dihydroxyvitamin D3 (1,25D) treatment improves HGPS phenotypes, including nuclear morphological abnormalities, DNA repair defects, and premature senescence. Importantly, we discovered that the 1,25D/VDR axis regulates LMNA gene expression, as well as expression of DNA repair factors. 1,25D dramatically reduces progerin production in HGPS cells, while stabilizing BRCA1 and 53BP1, two key factors for genome integrity. Vitamin D/VDR axis emerges as a new target for treatment of HGPS and potentially other lamin-related diseases exhibiting VDR deficiency and genomic instability. Because progerin expression increases with age, maintaining vitamin D/VDR signaling could keep the levels of progerin in check during physiological 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.