ArticleCirculation2021
Cardiovascular Progerin Suppression and Lamin A Restoration Rescue Hutchinson-Gilford Progeria Syndrome.
Article in Circulation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 42 citations in OpenAlex.
- cTAGE5/MEA6 Regulates LBR Localization to Maintain Nuclear Envelope Integrity and Safeguard Against Aging.Aging cell · 2025Article
- The accumulation of progerin underlies the loss of aortic smooth muscle cells in Hutchinson-Gilford progeria syndrome.Cell death & disease · 2025Article
- Anti-senescence therapies: a new concept to address cardiovascular disease.Cardiovascular research · 2025Review
- Endothelial cell-specific progerin expression does not cause cardiovascular alterations and premature death.Aging cell · 2025Article
- iSanXoT: A standalone application for the integrative analysis of mass spectrometry-based quantitative proteomics data.Computational and structural biotechnology journal · 2024Article
- Roles of the lamin A-specific tail region in the localization to sites of nuclear envelope rupture.PNAS nexus · 2024Article
- Nuclear envelope budding inhibition slows down progerin-induced aging process.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Endothelial YAP/TAZ activation promotes atherosclerosis in a mouse model of Hutchinson-Gilford progeria syndrome.The Journal of clinical investigation · 2024Article
- Senescent endothelial cells promote pathogenic neutrophil trafficking in inflamed tissues.EMBO reports · 2024Article
- Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model.International journal of molecular sciences · 2024Article
- Progerin forms an abnormal meshwork and has a dominant-negative effect on the nuclear lamina.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Exacerbated atherosclerosis in progeria is prevented by progerin elimination in vascular smooth muscle cells but not endothelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Coronary and carotid artery dysfunction and KGeroScience · 2024Article
- Hutchinson-Gilford progeria patient-derived cardiomyocyte model of carrying LMNA gene variant c.1824 C > T.Cell and tissue research · 2023Article
- Progerin, an Aberrant Spliced Form of Lamin A, Is a Potential Therapeutic Target for HGPS.Cells · 2023Review
- Biomechanical and transcriptional evidence that smooth muscle cell death drives an osteochondrogenic phenotype and severe proximal vascular disease in progeria.Biomechanics and modeling in mechanobiology · 2023Article
- Smooth Muscle Cell Death Drives an Osteochondrogenic Phenotype and Severe Proximal Vascular Disease in Progeria.bioRxiv : the preprint server for biology · 2023Article
- STAT1 Drives the Interferon-Like Response and Aging Hallmarks in Progeria.Aging biology · 2023Article
- Cellular Biomechanic Impairment in Cardiomyocytes Carrying the Progeria Mutation: An Atomic Force Microscopy Investigation.Langmuir : the ACS journal of surfaces and colloids · 2022Article
- Quantification of Farnesylated Progerin in Hutchinson-Gilford Progeria Patient Cells by Mass Spectrometry.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundHutchinson-Gilford progeria syndrome (HGPS) is a rare disorder characterized by premature aging and death mainly because of myocardial infarction, stroke, or heart failure. The disease is provoked by progerin, a variant of lamin A expressed in most differentiated cells. Patients look healthy at birth, and symptoms typically emerge in the first or second year of life. Assessing the reversibility of progerin-induced damage and the relative contribution of specific cell types is critical to determining the potential benefits of late treatment and to developing new therapies.
methodsWe used CRISPR-Cas9 technology to generate
resultsLike patients with HGPS,
conclusions
Indexed as
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.