ArticleRedox biology2024
Activation of nuclear receptor pregnane-X-receptor protects against abdominal aortic aneurysm by inhibiting oxidative stress.
Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Nicotinamide adenine dinucleotide phosphate hydrogen oxidase 2 exacerbates abdominal aortic aneurysm formation by inducing oxidative stress through autophagy inhibition.Histology and histopathology · 2026Article
- SERCA2 gatekeeper role in aortic autophagy: targeting the CaActa pharmacologica Sinica · 2026Article
- Integrated multi-omics analysis reveals a gut microbiota-tryptophan metabolism axis contributes to sex differences in a β-aminopropionitrile-induced aortic dissection mouse model.Biology of sex differences · 2026Article
- Review
- Global Profiling of the Proteome and Acetylome in Mice with Abdominal Aortic Aneurysms.ACS omega · 2025Article
- Neutrophils in inflammatory bowel disease: disease-promoting versus protective functions.Frontiers in immunology · 2025Review
- Identification of ARHGAP9 as a Key Diagnostic Marker for Abdominal Aortic Aneurysm by Multiomics and Experimental Validation.Human mutation · 2025Article
- Harnessing the therapeutic value of Tanshinone IIA: a breakthrough therapy in cardiovascular diseases.Frontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abdominal aortic aneurysm (AAA) is a life-threatening condition, but effective medications to prevent its progression and rupture are currently lacking. The nuclear receptor pregnane-X-receptor (PXR) plays a crucial role in vascular homeostasis. However, the role of PXR in AAA development remains unknown. We first detected the PXR expression in human and murine AAA tissues by RT-qPCR and Western blot. To investigate the potential role of PXR in the development of AAA, we used adeno-associated virus-mediated overexpression of PXR and pharmacological activation of PXR by ginkgolide A (GA) in mouse AAA models induced by both angiotensin II (AngII) and calcium phosphate [Ca
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