ArticleAging biology2023
STAT1 Drives the Interferon-Like Response and Aging Hallmarks in Progeria.
Article in Aging biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
12 citing papers in PubMed.
- Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.Nucleus (Austin, Tex.) · 2026Article
- Progerin Hinders Autophagy Flux at Its Final Stages in Hutchinson-Gilford Progeria Syndrome Cells, Preventing Its Own Autophagic Degradation.Aging cell · 2026Article
- Review
- A toxic STING-SAMHD1 axis drives replication stress in progeria and cancer cells.Nucleic acids research · 2026Article
- STING causes replication stress and nascent DNA degradation via SAMHD1.bioRxiv : the preprint server for biology · 2026Article
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- Baricitinib Augments Lonafarnib Therapy to Preserve Colonic Homeostasis and Microbial Balance in a Mouse Model of Progeria.Aging cell · 2025Article
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- Integrated single-cell multi-omics profiling reveals a senescence-associated hematopoietic landscape and regulatory network in aging bone marrow.Biogerontology · 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
- Fate-mapping and functional dissection reveal perilous influence of type I interferon signaling in mouse brain aging.Molecular neurodegeneration · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Hutchinson-Gilford progeria syndrome (HGPS), a devastating premature aging disease caused by the mutant lamin-A protein "progerin," features robust sterile inflammation/interferon (IFN)-like response. Targeting inflammation delays cellular and organismal HGPS phenotypes. However, specific mechanisms driving the sterile inflammation/IFN-like response and how this response causes tissue degeneration/loss in HGPS are unknown. We demonstrate that signal transducer and activator of transcription 1 (STAT1) drives the IFN-like response and aging phenotypes in HGPS cellular and mouse models. Calcitriol and baricitinib strongly repress sterile inflammation/IFN-like response, improving hallmarks of progerin-expressing cells such as mitochondrial, autophagy, and proliferation defects.
Identifiers
What OpenQuestion holds
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.