ArticleBMC medicine2023
Tomo-seq identifies NINJ1 as a potential target for anti-inflammatory strategy in thoracic aortic dissection.
Article in BMC medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 14 citations in OpenAlex.
- NINJ1 plays a vital role in the release of neutrophil extracellular traps during acute lung injury.Cell death & disease · 2026Article
- The role of NINJ1 in diseases.Cell death discovery · 2026Review
- Ninjurin1 in cardiovascular and vascular biology: From molecular mechanisms to therapeutic opportunities.Clinical and translational medicine · 2026Review
- Digging deeper into NINJ1: its multifaceted role in central nervous system diseases.Frontiers in immunology · 2026Review
- Aortic dissection as a disease of vascular wall homeostasis: integrating vasa vasorum-inflammation-metabolism axis for mechanistic insight and clinical translation.Frontiers in immunology · 2026Review
- Research Progress of Nerve Injury-Induced Protein 1 in Cardiovascular Diseases.Cardiology research and practice · 2026Review
- Article
- Plasma CCL3 predicts adverse heart failure outcomes in patients with arrhythmogenic cardiomyopathy.BMC medicine · 2025Article
- Targeting NINJ1-mediated cell rupture to treat inflammatory diseases.Molecular medicine (Cambridge, Mass.) · 2025Review
- Multifaceted roles of ninjurin1 in immunity, cell death, and disease.Frontiers in immunology · 2025Review
- Application of Spatial Omics in the Cardiovascular System.Research (Washington, D.C.) · 2025Review
- Enhanced expression of miR-20a driven by nanog exacerbated the degradation of extracellular matrix in thoracic aortic dissection.Non-coding RNA research · 2024Article
- NINJ1: Bridging lytic cell death and inflammation therapy.Cell death & disease · 2024Article
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThoracic aortic dissection (TAD) is a life-threatening disease caused by an intimal tear in the aorta. The histological characteristics differ significantly between the tear area (TA) and the distant area. Previous studies have emphasized that certain specific genes tend to cluster at the TA. Obtaining a thorough understanding of the precise molecular signatures near the TA will assist in discovering therapeutic strategies for TAD.
methodsWe performed a paired comparison of the pathological patterns in the TA with that in the remote area (RA). We used Tomo-seq, genome-wide transcriptional profiling with spatial resolution, to obtain gene expression signatures spanning from the TA to the RA. Samples from multiple sporadic TAD patients and animal models were used to validate our findings.
resultsPathological examination revealed that the TA of TAD exhibited more pronounced intimal hyperplasia, media degeneration, and inflammatory infiltration compared to the RA. The TA also had more apoptotic cells and CD31
conclusionsOur study showed that Tomo-seq had the advantage of obtaining spatial expression information of TAD across the TA and the RA. We pointed out that NINJ1 may be involved in inflammation and tissue remodeling, which played an important role in the formation of TAD. NINJ1 may serve as a potential therapeutic target for TAD.
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