ArticleJCI insight2018
LNK deficiency promotes acute aortic dissection and rupture.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Lnk deficiency attenuates the immunosuppressive capacity of MDSCs via ferroptosis to suppress tumor development.Cell death & disease · 2025Article
- CCDC80 Protects against Aortic Dissection and Rupture by Maintaining the Contractile Smooth Muscle Cell Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Recommendations for Design, Execution, and Reporting of Studies on Experimental Thoracic Aortopathy in Preclinical Models.Arteriosclerosis, thrombosis, and vascular biology · 2025Review
- LNK/SH2B3 loss of function increases susceptibility to murine and human atrial fibrillation.Cardiovascular research · 2024Article
- The role of longevity-related genetic variant interactions as predictors of survival after 85 years of age.Mechanisms of ageing and development · 2024Article
- Rare SH2B3 coding variants in lupus patients impair B cell tolerance and predispose to autoimmunity.The Journal of experimental medicine · 2024Article
- Comprehensive Analysis of Key m6A Modification Related Genes and Immune Infiltrates in Human Aortic Dissection.Frontiers in cardiovascular medicine · 2022Article
- Germline risk of clonal haematopoiesis.Nature reviews. Genetics · 2021Review
- The genetic architecture of plasma kynurenine includes cardiometabolic disease mechanisms associated with the SH2B3 gene.Scientific reports · 2021Article
- The Longevity-Associated SH2B3 (LNK) Genetic Variant: Selected Aging Phenotypes in 379,758 Subjects.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Article
- Multimodality Imaging-Based Characterization of Regional Material Properties in a Murine Model of Aortic Dissection.Scientific reports · 2020Article
- The genetics of human ageing.Nature reviews. Genetics · 2020Review
- Adaptor protein LNK promotes anaplastic thyroid carcinoma cell growth via 14-3-3 ε/γ binding.Cancer cell international · 2020Article
- LNK promotes the growth and metastasis of triple negative breast cancer via activating JAK/STAT3 and ERK1/2 pathway.Cancer cell international · 2020Article
- Critical role of Interleukin 21 and T follicular helper cells in hypertension and vascular dysfunction.JCI insight · 2019Article
- Early pathological characterization of murine dissecting abdominal aortic aneurysms.APL bioengineering · 2018Article
Corrections and comments
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Authors and funding
20 authors at 8 institutions in 3 countries.
Funding
Abstract
Aortic dissection (AD) is a life-threatening vascular disease with limited treatment strategies. Here, we show that loss of the GWAS-identified SH2B3 gene, encoding lymphocyte adaptor protein LNK, markedly increases susceptibility to acute AD and rupture in response to angiotensin (Ang) II infusion. As early as day 3 following Ang II infusion, prior to the development of AD, Lnk-/- aortas display altered mechanical properties, increased elastin breaks, collagen thinning, enhanced neutrophil accumulation, and increased MMP-9 activity compared with WT mice. Adoptive transfer of Lnk-/- leukocytes into Rag1-/- mice induces AD and rupture in response to Ang II, demonstrating that LNK deficiency in hematopoietic cells plays a key role in this disease. Interestingly, treatment with doxycycline prevents the early accumulation of aortic neutrophils and significantly reduces the incidence of AD and rupture. PrediXcan analysis in a biobank of more than 23,000 individuals reveals that decreased expression of SH2B3 is significantly associated with increased frequency of AD-related phenotypes (odds ratio 0.81). Thus, we identified a role for LNK in the pathology of AD in experimental animals and humans and describe a new model that can be used to inform both inherited and acquired forms of this disease.
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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.