ArticlePloS one2012
Cardiomyocyte-specific expression of lamin a improves cardiac function in Lmna-/- mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Review
- Lamin A/C Expression in Hematopoietic Cells Declines During Human Aging and Constrains Atherosclerosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- The Pathogenic Mechanisms of and Novel Therapies for Lamin A/C-Related Dilated Cardiomyopathy Based on Patient-Specific Pluripotent Stem Cell Platforms and Animal Models.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023Review
- Systematic in vivo candidate evaluation uncovers therapeutic targets for LMNA dilated cardiomyopathy and risk of Lamin A toxicity.Journal of translational medicine · 2023Article
- Lamin A/C Ablation Restricted to Vascular Smooth Muscle Cells, Cardiomyocytes, and Cardiac Fibroblasts Causes Cardiac and Vascular Dysfunction.International journal of molecular sciences · 2023Article
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- RNA Sequence Analyses throughout the Course of Mouse Cardiac Laminopathy Identify Differentially Expressed Genes for Cell Cycle Control and Mitochondrial Function.Scientific reports · 2020Article
- Postnatal development of mice with combined genetic depletions of lamin A/C, emerin and lamina-associated polypeptide 1.Human molecular genetics · 2019Article
- Ablation of SUN2-containing LINC complexes drives cardiac hypertrophy without interstitial fibrosis.Molecular biology of the cell · 2019Article
- Updated clinical overview on cardiac laminopathies: an electrical and mechanical disease.Nucleus (Austin, Tex.) · 2018Review
- The Pathogenesis and Therapies of Striated Muscle Laminopathies.Frontiers in physiology · 2018Review
- Lamin A/C Cardiomyopathies: Current Understanding and Novel Treatment Strategies.Current treatment options in cardiovascular medicine · 2017Review
- Current insights into LMNA cardiomyopathies: Existing models and missing LINCs.Nucleus (Austin, Tex.) · 2017Review
- Evidence that S6K1, but not 4E-BP1, mediates skeletal muscle pathology associated with loss of A-type lamins.Cell discovery · 2017Article
- Proteomic and phosphoproteomic analysis of renal cortex in a salt-load rat model of advanced kidney damage.Scientific reports · 2016Article
- How the proteome packages the genome for cardiovascular development.Proteomics · 2014Review
- Salt-induced changes in cardiac phosphoproteome in a rat model of chronic renal failure.PloS one · 2014Article
- Defective skeletal muscle growth in lamin A/C-deficient mice is rescued by loss of Lap2α.Human molecular genetics · 2013Article
- Phosphorylation of connexin43 on S279/282 may contribute to laminopathy-associated conduction defects.Experimental cell research · 2013Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Lmna(-/-) mice display multiple tissue defects and die by 6-8 weeks of age reportedly from dilated cardiomyopathy with associated conduction defects. We sought to determine whether restoration of lamin A in cardiomyocytes improves cardiac function and extends the survival of Lmna(-/-) mice. We observed increased total desmin protein levels and disorganization of the cytoplasmic desmin network in ~20% of Lmna(-/-) ventricular myocytes, rescued in a cell-autonomous manner in Lmna(-/-) mice expressing a cardiac-specific lamin A transgene (Lmna(-/-); Tg). Lmna(-/-); Tg mice displayed significantly increased contractility and preservation of myocardial performance compared to Lmna(-/-) mice. Lmna(-/-); Tg mice attenuated ERK1/2 phosphorylation relative to Lmna(-/-) mice, potentially underlying the improved localization of connexin43 to the intercalated disc. Electrocardiographic recordings from Lmna(-/-) mice revealed arrhythmic events and increased frequency of PR interval prolongation, which is partially rescued in Lmna(-/-); Tg mice. These findings support our observation that Lmna(-/-); Tg mice have a 12% median extension in lifespan compared to Lmna(-/-) mice. While significant, Lmna(-/-); Tg mice only have modest improvement in cardiac function and survival likely stemming from the observation that only 40% of Lmna(-/-); Tg cardiomyocytes have detectable lamin A expression. Cardiomyocyte-specific restoration of lamin A in Lmna(-/-) mice improves heart-specific pathology and extends lifespan, demonstrating that the cardiac pathology of Lmna(-/-) mice limits survival. The expression of lamin A is sufficient to rescue certain cellular defects associated with loss of A-type lamins in cardiomyocytes in a cell-autonomous fashion.
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Registered trials
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