ArticleNature cardiovascular research2025
Microtubule forces drive nuclear damage in LMNA cardiomyopathy.
Article in Nature cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- The nucleus as a mechanobiological hub in muscle aging.Nucleus (Austin, Tex.) · 2026Review
- Nuclear mechanobiology: a brief history and five unresolved questions.Nucleus (Austin, Tex.) · 2026Article
- 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
- Lamins gate nuclear and chromatin structures for cardiomyocyte maturation genes.bioRxiv : the preprint server for biology · 2026Article
- Microcephaly-associated genes asp and Sas4 influence chromatin organization and nuclear lamina structure in Drosophila melanogaster.Development (Cambridge, England) · 2026Article
- Emerin is necessary for microtubule-organizing center translocation to the nuclear envelope of muscle cells.Cell death & disease · 2026Article
- Review
- The cytoskeleton contributes to abnormal genome-lamina interactions in LMNA-deficient cardiomyocytes.The Journal of cell biology · 2026Article
- Nuclear Lamins: A Molecular Bridge Coupling Extracellular Mechanical Cues to Intranuclear Signal Transduction and Gene Regulation.International journal of molecular sciences · 2026Review
- A-type lamins anchor emerin at the inner nuclear membrane via two independent binding sites.The Journal of biological chemistry · 2026Article
- Nuclear Mechanotransduction at the Crossroads: How Membrane Receptors Remodel the Perinuclear Cytoskeleton to Drive Cancer and Disease.International journal of biological sciences · 2026Review
- Mechanical regulation of LINC complex function: structural basis, physiological roles, and disease mechanisms in transnuclear mechanotransduction.Frontiers in cell and developmental biology · 2026Review
- Constitutive heterochromatin controls nuclear mechanics, morphology, and integrity through H3K9me3 mediated chromocenter compaction.Nucleus (Austin, Tex.) · 2025Article
- Lamin variants cause cardiac arrhythmogenicity in Drosophila.Disease models & mechanisms · 2025Article
- Dysfunctional cardiomyocyte signalling and heart disease.Current opinion in cell biology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
Nuclear homeostasis requires balanced forces between the cytoskeleton and the nucleus. Mutations in LMNA, which encodes lamin A/C, weaken the nuclear lamina, leading to nuclear damage and muscle disease. Disrupting the linker of nucleoskeleton and cytoskeleton (LINC) complex, which connects the cytoskeleton to the nucleus, may ameliorate LMNA-associated cardiomyopathy, yet the cardioprotective mechanism remains unclear. Here we developed an assay to quantify the coupling between cardiomyocyte contraction and nuclear deformation and interrogate its dependence on the nuclear lamina and LINC complex. The LINC complex was mostly dispensable for transferring contractile strain to the nucleus, and its disruption did not rescue elevated nuclear strain in lamin A/C-deficient cardiomyocytes. Instead, LINC complex disruption eliminated the microtubule cage encircling the nucleus. Microtubule disruption prevented nuclear damage and preserved cardiac function in lamin A/C deficiency. Computational modeling revealed that microtubule forces create local stress concentrations that damage lamin A/C-deficient nuclei. These findings identify microtubule-dependent force transmission as a pathological driver and therapeutic target for LMNA cardiomyopathy.
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