ArticleInternational journal of clinical and experimental pathology2018
Gadd153 deficiency attenuates abdominal aortic aneurysm formation in mice.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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1 citing paper in PubMed, 1 citations in OpenAlex.
- SMOC2 promoted vascular smooth muscle cell proliferation, migration, and extracellular matrix degradation by activating BMP/TGF-β1 signaling pathway.Journal of clinical biochemistry and nutrition · 2023Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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Abstract
Abdominal aortic aneurysms (AAAs) are a chronic inflammatory vascular disease for which pharmacological treatments are not available. Gadd153 is closely associated with the onset of vascular smooth muscle cells (VSMCs) apoptosis. However, a role for Gadd153 in AngII-induced AAA formation is currently unknown. In our study, lentiviral-mediated silencing of Gadd153 through small RNA interference was performed in mice, which was further used for the establishment of mouse experimental AAA induced by infusion of angiotensin II (AngII). We found that Gadd153 deficiency prevented AngII-induced AAA formation in mice 14 days post perfusion compared with wild-type control mice. Moreover, Gadd153 deficiency significantly reduced lesion macrophage and CD4+ T-cell content, T-cell proliferation, SMC apoptosis, and matrix metalloproteinase expression.
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Identifiers
31938098PMC6957950W3011160366What OpenQuestion holds
Registered trials
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