ArticleMethods (San Diego, Calif.)2016
A high-content imaging-based screening pipeline for the systematic identification of anti-progeroid compounds.
Article in Methods (San Diego, Calif.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 61 citations in OpenAlex.
- Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.Nucleus (Austin, Tex.) · 2026Article
- Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming.Nature metabolism · 2026Article
- Prematurely Aged Human Microglia Exhibit Impaired Stress Response and Defective Nucleocytoplasmic Shuttling of ALS Associated FUS.Aging cell · 2025Article
- Transcriptional profiling of Hutchinson-Gilford Progeria patients identifies primary target pathways of progerin.bioRxiv : the preprint server for biology · 2025Article
- A noncanonical cGAS-STING pathway drives cellular and organismal aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mechanotransduction for therapeutic approaches: Cellular aging and rejuvenation.APL bioengineering · 2025Review
- Revisiting the approaches to DNA damage detection in genetic toxicology: insights and regulatory implications.BioData mining · 2025Article
- Review
- A multiparametric screen uncovers FDA-approved small molecules that potentiate the nuclear mechano-dysfunctions in ATR-defective cells.Scientific reports · 2024Article
- Senescent endothelial cells promote pathogenic neutrophil trafficking in inflamed tissues.EMBO reports · 2024Article
- p300 nucleocytoplasmic shuttling underlies mTORC1 hyperactivation in Hutchinson-Gilford progeria syndrome.Nature cell biology · 2024Article
- Activation of endoplasmic reticulum stress in premature aging via the inner nuclear membrane protein SUN2.Cell reports · 2023Article
- Systematic estimation of biological age ofFrontiers in aging · 2023Article
- Unsupervised discovery of dynamic cell phenotypic states from transmitted light movies.PLoS computational biology · 2021Article
- Small-Molecule Therapeutic Perspectives for the Treatment of Progeria.International journal of molecular sciences · 2021Review
- Systematic screening identifies therapeutic antisense oligonucleotides for Hutchinson-Gilford progeria syndrome.Nature medicine · 2021Article
- Computational Methods for Single-Cell Imaging and Omics Data Integration.Frontiers in molecular biosciences · 2021Review
- Impairment of nuclear F-actin formation and its relevance to cellular phenotypes in Hutchinson-Gilford progeria syndrome.Nucleus (Austin, Tex.) · 2020Article
- Article
- Nuclear Organization in Stress and Aging.Cells · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is an early onset lethal premature aging disorder caused by constitutive production of progerin, a mutant form of the nuclear architectural protein lamin A. The presence of progerin causes extensive morphological, epigenetic and DNA damage related nuclear defects that ultimately disrupt tissue and organismal functions. Hypothesis-driven approaches focused on HGPS affected pathways have been used in attempts to identify druggable targets with anti-progeroid effects. Here, we report an unbiased discovery approach to HGPS by implementation of a high-throughput, high-content imaging based screening method that enables systematic identification of small molecules that prevent the formation of multiple progerin-induced aging defects. Screening a library of 2816 FDA approved drugs, we identified retinoids as a novel class of compounds that reverses aging defects in HGPS patient skin fibroblasts. These findings establish a novel approach to anti-progeroid drug discovery.
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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.