ArticleMolecular biology of the cell2019
Ablation of SUN2-containing LINC complexes drives cardiac hypertrophy without interstitial fibrosis.
Article in Molecular biology of the cell, 2019. 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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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- The nucleus as a mechanobiological hub in muscle aging.Nucleus (Austin, Tex.) · 2026Review
- Nuclear SUN2 coordinates endothelial cell-matrix interactions to regulate blood vessel homeostasis and barrier function.Angiogenesis · 2026Article
- Loss ofbioRxiv : the preprint server for biology · 2026Article
- SUN2 mediates epigenetic remodeling to drive mechanotransduction during skin fibrosis.bioRxiv : the preprint server for biology · 2026Article
- Prioritization of causal genes from genome-wide association studies by Bayesian data integration across loci.PLoS computational biology · 2025Article
- Nuclear envelope proteins, mechanotransduction, and their contribution to breast cancer progression.npj biological physics and mechanics · 2025Review
- Modelling and targeting mechanical forces in organ fibrosis.Nature reviews bioengineering · 2024Article
- The molecular mechanism of MiR-26a-5p regulates autophagy and activates NLRP3 inflammasome to mediate cardiomyocyte hypertrophy.BMC cardiovascular disorders · 2024Article
- Life at the crossroads: the nuclear LINC complex and vascular mechanotransduction.Frontiers in physiology · 2024Review
- Lem2 is essential for cardiac development by maintaining nuclear integrity.Cardiovascular research · 2023Article
- A membrane-sensing mechanism links lipid metabolism to protein degradation at the nuclear envelope.The Journal of cell biology · 2023Article
- Disulfide bond in SUN2 regulates dynamic remodeling of LINC complexes at the nuclear envelope.Life science alliance · 2023Article
- Transgenic force sensors and software to measure force transmission across the mammalian nuclear envelope in vivo.Biology open · 2022Article
- Identification of candidate biomarkers and pathways associated with type 1 diabetes mellitus using bioinformatics analysis.Scientific reports · 2022Article
- Nuclear Mechanosensation and Mechanotransduction in Vascular Cells.Frontiers in cell and developmental biology · 2022Review
- SARS-CoV-2 infection of human iPSC-derived cardiac cells reflects cytopathic features in hearts of patients with COVID-19.Science translational medicine · 2021Article
- Nucleus Type-Specific DNA Methylomics Reveals Epigenetic "Memory" of Prior Adaptation in Skeletal Muscle.Function (Oxford, England) · 2021Article
- The LINC Between Mechanical Forces and Chromatin.Frontiers in physiology · 2021Review
- SARS-CoV-2 infection of human iPSC-derived cardiac cells predicts novel cytopathic features in hearts of COVID-19 patients.bioRxiv : the preprint server for biology · 2020Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The cardiomyocyte cytoskeleton, including the sarcomeric contractile apparatus, forms a cohesive network with cellular adhesions at the plasma membrane and nuclear--cytoskeletal linkages (LINC complexes) at the nuclear envelope. Human cardiomyopathies are genetically linked to the LINC complex and A-type lamins, but a full understanding of disease etiology in these patients is lacking. Here we show that SUN2-null mice display cardiac hypertrophy coincident with enhanced AKT/MAPK signaling, as has been described previously for mice lacking A-type lamins. Surprisingly, in contrast to lamin A/C-null mice, SUN2-null mice fail to show coincident fibrosis or upregulation of pathological hypertrophy markers. Thus, cardiac hypertrophy is uncoupled from profibrotic signaling in this mouse model, which we tie to a requirement for the LINC complex in productive TGFβ signaling. In the absence of SUN2, we detect elevated levels of the integral inner nuclear membrane protein MAN1, an established negative regulator of TGFβ signaling, at the nuclear envelope. We suggest that A-type lamins and SUN2 play antagonistic roles in the modulation of profibrotic signaling through opposite effects on MAN1 levels at the nuclear lamina, suggesting a new perspective on disease etiology.
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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.