ReviewMolecular neurobiology2018
Hutchinson-Gilford Progeria Syndrome: A Premature Aging Disease.
Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 114 citations in OpenAlex.
- First Generation Proteolysis Targeting Chimeras (PROTACs) for the Treatment of Progeria.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic Profiling Reveals Organ-Specific Molecular Pathologies and Aging-Associated Biomarkers in Progeroid Laminopathy.Smart medicine · 2026Article
- SASdb: a comprehensive database for sex-biased alternative splicing profiles in human tissues.Biology of sex differences · 2026Article
- Review
- A study on the nutritional status and body composition of children with Hutchinson-Gilford progeria syndrome.Orphanet journal of rare diseases · 2026Article
- Exploring the Therapeutic Potential of Plant-Based Natural Products in Combating Aging.Current drug targets · 2026Review
- Unraveling the mysteries of Hutchinson-Gilford progeria syndrome: a comprehensive review of LMNA gene mutations.Biogerontology · 2025Review
- National survey of Hutchinson-Gilford progeria syndrome and progeroid laminopathy in Japan.Aging · 2025Article
- Analyzing different aging theories in the context of the brain: DNA damage, inflammation, redox imbalance, and neurodevelopment intertwine.Biogerontology · 2025Review
- Review
- Review
- Comprehensive analysis of senescence-related genes identifies prognostic clusters with distinct characteristics in glioma.Scientific reports · 2025Article
- Integrative analysis of senescence-related genes identifies robust prognostic clusters with distinct features in hepatocellular carcinoma.Journal of advanced research · 2025Article
- Adenine base editing rescues pathogenic phenotypes in tissue engineered vascular model of Hutchinson-Gilford progeria syndrome.APL bioengineering · 2025Article
- Progerin mRNA Is Associated with Smoking and Signs of Increased Microvascular Damage in Patients with Diabetic Macular Edema.International journal of molecular sciences · 2025Article
- Regulated vascular smooth muscle cell death in vascular diseases.Cell proliferation · 2024Review
- BubR1 and SIRT2: Insights into aneuploidy, aging, and cancer.Seminars in cancer biology · 2024Review
- SpliceTransformer predicts tissue-specific splicing linked to human diseases.Nature communications · 2024Article
- Premature aging effects on COVID-19 pathogenesis: new insights from mouse models.Scientific reports · 2024Article
- Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Progeria is sporadic, very rare, autosomal dominant, deadly childhood disorder. It is one of the progeroid syndromes also known as Hutchinson-Gilford progeria syndrome (HGPS). Aging is a developmental process that begins with fertilization and ends up with death involving a lot of environmental and genetic factors. The disease firstly involves premature aging and then death from complications of atherosclerosis such as myocardial infarction, stroke, atherosclerosis, or heart failure. The lifespan of the patient is normally up to teen age or early twenties. It is usually not inherited because a patient normally dies before the age of reproduction. The most important genetic linkage between progeria and aging is shortening of telomere ends with each replication cycle. The patients are normally observed to have extremely short telomeres. Currently, 90% of the patients are said to have de novo point mutations in the LMNA gene that substitute cytosine with thymine and have been found in individuals with HGPS. Lmna encodes lamins A and C, and the A-type lamins have important structural function in the nuclear envelope. The most common type of HGPS mutation is located at codon 608 (G608G). It could not be diagnosed at birth, but after the age of 2 years, visible, prominent symptoms can be observed. Still, lot of research is needed to solve this mystery; hopefully, future research on HGPS would provide important clues for progeria and other fatal age-related disorders.
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.