ArticleNature communications2021
Disrupting the LINC complex by AAV mediated gene transduction prevents progression of Lamin induced cardiomyopathy.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.
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
62 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A common variant that alters SUN1 degradation associates with hepatic steatosis and metabolic traits in multiple cohorts.Journal of hepatology · 2023Pooled it
- Nuclear mechanobiology: a brief history and five unresolved questions.Nucleus (Austin, Tex.) · 2026Article
- The nucleus as a mechanobiological hub in muscle aging.Nucleus (Austin, Tex.) · 2026Review
- Nuclear envelope rupture and resealing: mechanisms, consequences, and disease implications.Biochemical Society transactions · 2026Review
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- NUAK1 Inhibition Alleviates Ischemia-Reperfusion Injury via SYNE1-YAP1.Circulation research · 2026Article
- Essential Role for Telomeric Repeat-Binding Factor 2 in Cardiac Development and Function.FASEB bioAdvances · 2026Article
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- Lamins gate nuclear and chromatin structures for cardiomyocyte maturation genes.bioRxiv : the preprint server for biology · 2026Article
- Review
- The cytoskeleton contributes to abnormal genome-lamina interactions in LMNA-deficient cardiomyocytes.The Journal of cell biology · 2026Article
- Telomere shortening in laminopathic dilated cardiomyopathy.NPJ Regenerative medicine · 2026Article
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of functionNucleus (Austin, Tex.) · 2025Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Microtubule forces drive nuclear damage in LMNA cardiomyopathy.Nature cardiovascular research · 2025Article
- The role of iPSC research for insight into inherited arrhythmia conditions.Heart rhythm · 2025Review
- A microtubule cage damages weakened nuclei in a genetic cardiomyopathy.Nature cardiovascular research · 2025Article
- Lamin A/C Expression in Hematopoietic Cells Declines During Human Aging and Constrains Atherosclerosis in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Profibrotic Molecules Are Reduced in CRISPR-Edited Emery-Dreifuss Muscular Dystrophy Fibroblasts.Cells · 2025Article
- Variant-Specific Late Gadolinium Enhancement Patterns Influence Clinical Outcomes inJournal of the American Heart Association · 2025Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the LaminA gene are a common cause of monogenic dilated cardiomyopathy. Here we show that mice with a cardiomyocyte-specific Lmna deletion develop cardiac failure and die within 3-4 weeks after inducing the mutation. When the same Lmna mutations are induced in mice genetically deficient in the LINC complex protein SUN1, life is extended to more than one year. Disruption of SUN1's function is also accomplished by transducing and expressing a dominant-negative SUN1 miniprotein in Lmna deficient cardiomyocytes, using the cardiotrophic Adeno Associated Viral Vector 9. The SUN1 miniprotein disrupts binding between the endogenous LINC complex SUN and KASH domains, displacing the cardiomyocyte KASH complexes from the nuclear periphery, resulting in at least a fivefold extension in lifespan. Cardiomyocyte-specific expression of the SUN1 miniprotein prevents cardiomyopathy progression, potentially avoiding the necessity of developing a specific therapeutic tailored to treating each different LMNA cardiomyopathy-inducing mutation of which there are more than 450.
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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 Socratic graph.