ArticleProceedings of the National Academy of Sciences of the United States of America2016
Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Ultrasonic Characteristics of Cardiovascular Changes in Children with Hutchinson-Gilford Progeria Syndrome: A Comparative Study with Normal Children and Aging People.BioMed research international · 2020Trial
- METTL14-Mediated mAging cell · 2026Article
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- Article
- Meis transcription factors regulate cardiac conduction system development and adult function.Cardiovascular research · 2025Article
- Disease pathogenicity in Hutchinson-Gilford progeria syndrome mice: insights from lung-associated alterations.Molecular medicine (Cambridge, Mass.) · 2025Article
- The Dental and Oral Significance of Hutchinson-Gilford Prfogeria Syndrome : The Dental and Oral Significance of Hutchinson-Gilford Prfogeria Syndrome.Galen medical journal · 2025Review
- Cardiac electrical abnormalities in a mouse model of left ventricular non-compaction cardiomyopathy.PloS one · 2025Article
- Angiopoietin-2: A Therapeutic Target for Vascular Protection in Hutchinson-Gilford Progeria Syndrome.International journal of molecular sciences · 2024Review
- The G4 resolvase Dhx36 modulates cardiomyocyte differentiation and ventricular conduction system development.Nature communications · 2024Article
- Cardiac and skeletal muscle manifestations in the G608G mouse model of Hutchinson-Gilford progeria syndrome.Aging cell · 2024Article
- Coronary and carotid artery dysfunction and KGeroScience · 2024Article
- p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia.Nature cardiovascular research · 2023Article
- Aging Model for Analyzing Drug-Induced Proarrhythmia Risks Using Cardiomyocytes Differentiated from Progeria-Patient-Derived Induced Pluripotent Stem Cells.International journal of molecular sciences · 2023Article
- Acute Coronary Syndrome Treated with Percutaneous Coronary Intervention in Hutchinson-Gilford Progeria.Children (Basel, Switzerland) · 2023Article
- Cellular Biomechanic Impairment in Cardiomyocytes Carrying the Progeria Mutation: An Atomic Force Microscopy Investigation.Langmuir : the ACS journal of surfaces and colloids · 2022Article
- Characterizing arrhythmia using machine learning analysis of CaStem cell reports · 2022Article
- Senescence mechanisms and targets in the heart.Cardiovascular research · 2022Review
- Paclitaxel mitigates structural alterations and cardiac conduction system defects in a mouse model of Hutchinson-Gilford progeria syndrome.Cardiovascular research · 2022Article
- Cardiovascular Progerin Suppression and Lamin A Restoration Rescue Hutchinson-Gilford Progeria Syndrome.Circulation · 2021Article
Corrections and comments
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Authors and funding
22 authors at 10 institutions in 2 countries.
Funding
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a rare genetic disease caused by defective prelamin A processing, leading to nuclear lamina alterations, severe cardiovascular pathology, and premature death. Prelamin A alterations also occur in physiological aging. It remains unknown how defective prelamin A processing affects the cardiac rhythm. We show age-dependent cardiac repolarization abnormalities in HGPS patients that are also present in the Zmpste24
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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.