ReviewNucleus (Austin, Tex.)2018
An overview of treatment strategies for Hutchinson-Gilford Progeria syndrome.
Review in Nucleus (Austin, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- Pooled it
- Patient-Derived Cortical Organoids Reveal Senescence of Neural Progenitor Cells in Hutchinson-Gilford Progeria Syndrome.Aging cell · 2025Article
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
- Enhancing Cellular Homeostasis: Targeted Botanical Compounds Boost Cellular Health Functions in Normal and Premature Aging Fibroblasts.Biomolecules · 2024Article
- The syntaxin-binding protein STXBP5 regulates progerin expression.Scientific reports · 2024Article
- Navigating Lipodystrophy: Insights from Laminopathies and Beyond.International journal of molecular sciences · 2024Review
- Mitophagy defect mediates the aging-associated hallmarks in Hutchinson-Gilford progeria syndrome.Aging cell · 2024Article
- Characterization of the craniofacial abnormalities of the homozygous G608G progeria mouse model.Frontiers in physiology · 2024Article
- The secretome atlas of two mouse models of progeria.Aging cell · 2023Article
- Article
- Article
- Progeria-a Rare Genetic Condition with Accelerated Ageing Process.Applied biochemistry and biotechnology · 2023Review
- In vivo stress reporters as early biomarkers of the cellular changes associated with progeria.Journal of cellular and molecular medicine · 2022Article
- Review
- Impact of MnTBAP and Baricitinib Treatment on Hutchinson-Gilford Progeria Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Rapid and robust derivation of mesenchymal stem cells from human pluripotent stem cells via temporal induction of neuralized ectoderm.Cell & bioscience · 2022Article
- MG132 Induces Progerin Clearance and Improves Disease Phenotypes in HGPS-like Patients' Cells.Cells · 2022Article
- Case report: Focal segmental glomerulosclerosis in a pediatric atypical progeroid syndrome.Frontiers in pediatrics · 2022Article
- Efficacy of Cord Blood Cell Therapy for Hutchinson-Gilford Progeria Syndrome-A Case Report.International journal of molecular sciences · 2021Article
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a sporadic, autosomal dominant disorder characterized by premature and accelerated aging symptoms leading to death at the mean age of 14.6 years usually due to cardiovascular complications. HGPS is caused by a de novo point mutation in the LMNA gene encoding the intermediate filament proteins lamins A and C which are structural components of the nuclear lamina. This mutation leads to the production of a truncated toxic form of lamin A, issued from aberrant splicing and called progerin. Progerin accumulates in HGPS cells' nuclei and is a hallmark of the disease. Small amounts of progerin are also produced during normal aging. HGPS cells and animal preclinical models have provided insights into the molecular and cellular pathways that underlie the disease and have also highlighted possible mechanisms involved in normal aging. This review reports recent medical advances and treatment approaches for patients affected with HGPS.
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.