ArticleNature communications2025
GSDME-dependent pyroptosis drives abdominal aortic aneurysm via promoting vascular senescence.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- PPARα activation overcomes fibroinflammatory liver microenvironment-associated anti-PD-1 resistance in hepatocellular carcinoma by mediating GSDME-dependent pyroptosis.Nature communications · 2026Article
- Targeting pyroptosis to treat aortic aneurysms: From mechanism to drug discovery (Review).International journal of molecular medicine · 2026Review
- The Metabolite Differences in Vascular Smooth Muscle Cells of Abdominal Aortic Aneurysm Revealed by Untargeted Metabolomics.Biomedicines · 2026Article
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Senescence contributes to the pathology of abdominal aortic aneurysm (AAA); however, the regulation of senescence in AAA remains unclear. Here, we sought to determine the role of gasdermin-E (GSDME)-dependent non-canonical pyroptosis in AAA. GSDME-dependent non-canonical pyroptosis is activated in the lesioned vascular walls of mouse models and patients with AAA. GSDME deficiency inhibits vascular senescence and AAA progression. Combined analyses of single-cell RNA sequencing (scRNA-seq), bulk RNA-seq, and multiplex flow cytometry demonstrate that GSDME is essential for the reprogramming of vascular smooth muscle cells (VSMCs) and the shift in immune statuses of macrophages, monocytes, and neutrophils in AAA. Reintroduction of GSDME in VSMCs, but not in myeloid cells, in mice with a GSDME deletion background, recapitulates the induced vascular senescence and AAA, which is abolished by senolytic therapy with dasatinib plus quercetin. These results indicate that GSDME-dependent non-canonical pyroptosis in VSMCs may be a 'master switch' in AAA and a potential therapeutic target for managing AAA.
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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.