ReviewCells2021
Molecular and Cellular Mechanisms Driving Cardiovascular Disease in Hutchinson-Gilford Progeria Syndrome: Lessons Learned from Animal Models.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.Nucleus (Austin, Tex.) · 2026Article
- Dysregulated lncRNAs are associated with the progressive arterial phenotype in Hutchinson-Gilford Progeria Syndrome.GeroScience · 2026Article
- Single-cell analysis of the progeria arterial wall reveals progerin-induced progressive, cell type-specific dysfunction and somatic mutation accumulation.Genome medicine · 2026Article
- The unfolded protein response in progeria arteries originates from non-endothelial cell types.Life science alliance · 2026Article
- Vascular adventitial cells and vascular remodeling: when a harp of thousand strings does not keep in tune so long.Frontiers in physiology · 2026Review
- Selection of specific and efficient siRNAs in new cellular model for Hutchinson-Gilford progeria syndrome therapy.Molecular therapy. Nucleic acids · 2025Article
- Sirtuins as Endogenous Regulators of Cardiac Fibrosis: A Current Perspective.Cardiovascular toxicology · 2025Review
- Transcriptional profiling of Hutchinson-Gilford Progeria patients identifies primary target pathways of progerin.bioRxiv : the preprint server for biology · 2025Article
- Impacts of Radiation on Metabolism and Vascular Cell Senescence.Antioxidants & redox signaling · 2025Review
- Perinatal Exposure to Lead or Diethylhexyl Phthalate in Mice: Sex-Specific Effects on Cardiac DNA Methylation and Gene Expression across Time.Environmental health perspectives · 2025Article
- Baricitinib and Lonafarnib Synergistically Target Progerin and Inflammation, Improving Lifespan and Health in Progeria Mice.International journal of molecular sciences · 2025Article
- Disease pathogenicity in Hutchinson-Gilford progeria syndrome mice: insights from lung-associated alterations.Molecular medicine (Cambridge, Mass.) · 2025Article
- Article
- Endothelial cell-specific progerin expression does not cause cardiovascular alterations and premature death.Aging cell · 2025Article
- Hutchinson-Gilford progeria syndrome alters the endothelial genetic response to laminar shear stress.Frontiers in physiology · 2025Article
- Enhancing Cellular Homeostasis: Targeted Botanical Compounds Boost Cellular Health Functions in Normal and Premature Aging Fibroblasts.Biomolecules · 2024Article
- Endothelial YAP/TAZ activation promotes atherosclerosis in a mouse model of Hutchinson-Gilford progeria syndrome.The Journal of clinical investigation · 2024Article
- Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model.International journal of molecular sciences · 2024Article
- Life at the crossroads: the nuclear LINC complex and vascular mechanotransduction.Frontiers in physiology · 2024Review
- Prelamin A and ZMPSTE24 in premature and physiological aging.Nucleus (Austin, Tex.) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disease that recapitulates many symptoms of physiological aging and precipitates death. Patients develop severe vascular alterations, mainly massive vascular smooth muscle cell loss, vessel stiffening, calcification, fibrosis, and generalized atherosclerosis, as well as electrical, structural, and functional anomalies in the heart. As a result, most HGPS patients die of myocardial infarction, heart failure, or stroke typically during the first or second decade of life. No cure exists for HGPS, and therefore it is of the utmost importance to define the mechanisms that control disease progression in order to develop new treatments to improve the life quality of patients and extend their lifespan. Since the discovery of the HGPS-causing mutation, several animal models have been generated to study multiple aspects of the syndrome and to analyze the contribution of different cell types to the acquisition of the HGPS-associated cardiovascular phenotype. This review discusses current knowledge about cardiovascular features in HGPS patients and animal models and the molecular and cellular mechanisms through which progerin causes cardiovascular disease.
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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.