ReviewNucleus (Austin, Tex.)2017
Current insights into LMNA cardiomyopathies: Existing models and missing LINCs.
Review in Nucleus (Austin, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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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.
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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
49 citing papers in PubMed, 67 citations in OpenAlex.
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of functionNucleus (Austin, Tex.) · 2025Review
- Cardiac phenotypes in LMNA mutations.Current opinion in cardiology · 2025Review
- AFrontiers in genetics · 2025Article
- Response to Letter to the Editor: "How to Screen and Manage Suspected Laminopathy".Internal medicine (Tokyo, Japan) · 2025Article
- Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model.International journal of molecular sciences · 2024Article
- Eliminating elevated p53 signaling fails to rescue skeletal muscle defects or extend survival in lamin A/C-deficient mice.Cell death discovery · 2024Article
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- A Clinical Diagnosis of Laminopathy without Systolic Dysfunction: When Does Nuclei Malformation Start?Internal medicine (Tokyo, Japan) · 2024Article
- p38γ/δ activation alters cardiac electrical activity and predisposes to ventricular arrhythmia.Nature cardiovascular research · 2023Article
- Article
- AAV9-mediated SMN gene therapy rescues cardiac desmin but not lamin A/C and elastin dysregulation in Smn2B/- spinal muscular atrophy mice.Human molecular genetics · 2023Article
- VEGF-B hypertrophy predisposes to transition from diastolic to systolic heart failure in hypertensive rats.Cardiovascular research · 2023Article
- Epigenetics inCells · 2023Review
- Nesprin-1 LINC complexes recruit microtubule cytoskeleton proteins and drive pathology in Lmna-mutant striated muscle.Human molecular genetics · 2023Article
- Comprehensive review on gene mutations contributing to dilated cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- Genomic analysis of a novel pathogenic variant in the gene LMNA associated with cardiac laminopathies found in Ecuadorian siblings: A case report.Frontiers in cardiovascular medicine · 2023Article
- Cardiovascular aging: from cellular and molecular changes to therapeutic interventions.The journal of cardiovascular aging · 2023Article
- Novel pathogenic variant in LMNA gene identified in a six-generation family causing atrial cardiomyopathy and associated right atrial conduction arrhythmias.Frontiers in cardiovascular medicine · 2023Article
- Massively Parallel Sequencing of 43 Arrhythmia Genes in a Selected SUDI Cohort from Cape Town.Journal of pediatric genetics · 2022Article
- Pathogenesis of Cardiomyopathy Caused by Variants inCirculation · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The nuclear lamina is a critical structural domain for the maintenance of genomic stability and whole-cell mechanics. Mutations in the LMNA gene, which encodes nuclear A-type lamins lead to the disruption of these key cellular functions, resulting in a number of devastating diseases known as laminopathies. Cardiomyopathy is a common laminopathy and is highly penetrant with poor prognosis. To date, cell mechanical instability and dysregulation of gene expression have been proposed as the main mechanisms driving cardiac dysfunction, and indeed discoveries in these areas have provided some promising leads in terms of therapeutics. However, important questions remain unanswered regarding the role of lamin A dysfunction in the heart, including a potential role for the toxicity of lamin A precursors in LMNA cardiomyopathy, which has yet to be rigorously investigated.
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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.