ArticleCommunications medicine2025
Hydrogen sulfide aggravates neutrophil infiltration, vascular remodeling and elastase-induced abdominal aortic aneurysm in male mice.
Article in Communications medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Metabolic reprogramming in aortic diseases: insights from metabolomics and therapeutic opportunities.Medical review (2021) · 2026Review
- Reactive sulfur species as emerging immunomodulators: mechanistic insights and therapeutic prospects.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundAbdominal aortic aneurysm (AAA) has an 80% mortality rate upon rupture, with no pharmacological treatments available to slow its progression. Hydrogen sulfide (H₂S), produced by cystathionine γ-lyase (CSE), has anti-inflammatory and antioxidant properties, but its role in AAA remains unclear.
methodsWe evaluated the impact of sodium thiosulfate (STS), a clinically relevant H₂S donor, in a periadventitial elastase-induced AAA model in normotensive male wild-type and Cse
resultsContrary to expectations, STS dose-dependently aggravate AAA progression by increasing extracellular matrix degradation. Although STS reduces macrophage and lymphocyte infiltration, it enhances neutrophil accumulation, particularly MMP9⁺ neutrophils, and promotes the formation of c-KIT⁺-MPO⁺ pre-neutrophil clusters. Cse
conclusionsH₂S, delivered via STS, exacerbates AAA progression under normotensive conditions by promoting neutrophil-driven inflammation and impairing VSMC repair. These findings challenge the assumption that H₂S is universally protective in vascular disease and raise caution regarding the therapeutic use of STS in patients at risk for AAA.
Identifiers
What Socratic holds
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.