ArticleCardiovascular research2018
Biomechanical defects and rescue of cardiomyocytes expressing pathologic nuclear lamins.
Article in Cardiovascular research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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
24 citing papers in PubMed, 54 citations in OpenAlex.
- High-Throughput Methods for Variant Functional Assessment in Cardiac Disease.Circulation. Genomic and precision medicine · 2026Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- Intracellular remodeling associated with endoplasmic reticulum stress modifies biomechanical compliance of bladder cells.Cell communication and signaling : CCS · 2023Article
- An alpha-helix variant p.Arg156Pro in LMNA as a cause of hereditary dilated cardiomyopathy: genetics and bioinfomatics exploration.BMC medical genomics · 2023Article
- 3D photopolymerized microstructured scaffolds influence nuclear deformation, nucleo/cytoskeletal protein organization, and gene regulation in mesenchymal stem cells.APL bioengineering · 2023Article
- Precision therapy in dilated cardiomyopathy: Pipedream or paradigm shift?Cambridge prisms. Precision medicine · 2023Review
- Cellular Biomechanic Impairment in Cardiomyocytes Carrying the Progeria Mutation: An Atomic Force Microscopy Investigation.Langmuir : the ACS journal of surfaces and colloids · 2022Article
- A comprehensive review of computational and image analysis techniques for quantitative evaluation of striated muscle tissue architecture.Biophysics reviews · 2022Review
- Atomic Force Microscopy (AFM) Applications in Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2022Review
- An LMNA synonymous variant associated with severe dilated cardiomyopathy: Case report.American journal of medical genetics. Part A · 2022Article
- Molecular rationale for SARS-CoV-2 spike circulating mutations able to escape bamlanivimab and etesevimab monoclonal antibodies.Scientific reports · 2021Article
- Compromised Biomechanical Properties, Cell-Cell Adhesion and Nanotubes Communication in Cardiac Fibroblasts Carrying the Lamin A/C D192G Mutation.International journal of molecular sciences · 2021Article
- p38 MAPKs - roles in skeletal muscle physiology, disease mechanisms, and as potential therapeutic targets.JCI insight · 2021Review
- Nuclear filaments: role in chromosomal positioning and gene expression.Nucleus (Austin, Tex.) · 2020Review
- Review
- Article
- Lamin A/C Cardiomyopathy: Implications for Treatment.Current cardiology reports · 2019Review
- Emery-Dreifuss muscular dystrophy: focal point nuclear envelope.Current opinion in neurology · 2019Review
- The structural and gene expression hypotheses in laminopathic diseases-not so different after all.Molecular biology of the cell · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
Aims: Given the clinical impact of LMNA cardiomyopathies, understanding lamin function will fulfill a clinical need and will lead to advancement in the treatment of heart failure. A multidisciplinary approach combining cell biology, atomic force microscopy (AFM), and molecular modeling was used to analyse the biomechanical properties of human lamin A/C gene (LMNA) mutations (E161K, D192G, N195K) using an in vitro neonatal rat ventricular myocyte model. Methods and results: The severity of biomechanical defects due to the three LMNA mutations correlated with the severity of the clinical phenotype. AFM and molecular modeling identified distinctive biomechanical and structural changes, with increasing severity from E161K to N195K and D192G, respectively. Additionally, the biomechanical defects were rescued with a p38 MAPK inhibitor. Conclusions: AFM and molecular modeling were able to quantify distinct biomechanical and structural defects in LMNA mutations E161K, D192G, and N195K and correlate the defects with clinical phenotypic severity. Improvements in cellular biomechanical phenotype was demonstrated and may represent a mechanism of action for p38 MAPK inhibition therapy that is now being used in human clinical trials to treat laminopathies.
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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.