ArticleCardiovascular drugs and therapy2025
Dexmedetomidine Alleviates Abdominal Aortic Aneurysm by Activating Autophagy Via AMPK/mTOR Pathway.
Article in Cardiovascular drugs and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 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
- GDF11 Regulates Vascular Smooth Muscle Cell Phenotype Switching to Prevent Aortic Aneurysm Formation.Cardiovascular drugs and therapy · 2026Article
- Therapeutic Strategies for Abdominal Aortic Aneurysm: A Comprehensive Systematic Review.Journal of cardiovascular development and disease · 2025Review
- Study on the mechanism of Dexmedetomidine's effect on postoperative cognitive dysfunction in elderly people.Frontiers in physiology · 2025Review
- Atractylenolide-I prevents abdominal aortic aneurysm formation through inhibiting inflammation.Frontiers in immunology · 2025Article
- Montelukast inhibits abdominal aortic aneurysm formation in mice via activating the AMPK/mTOR signalling pathway.Langenbeck's archives of surgery · 2024Article
- O304 alleviates abdominal aortic aneurysm formation via AMPK/mTOR/MMP pathway activation.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAbdominal aortic aneurysms (AAA) are a critical global health issue with increasing prevalence. Dexmedetomidine (DEX) is a highly selective α2-adrenoceptor agonist that has previously been shown to play a protective role in AAA. Nevertheless, the mechanisms underlying its protection effect remain not fully understood.
methodsA rat AAA model was established via intra-aortic porcine pancreatic elastase perfusion with or without DEX administration. The abdominal aortic diameters of rats were measured. Hematoxylin-eosin and Elastica van Gieson staining were conducted for histopathological observation. TUNEL and immunofluorescence staining were utilized to detect cell apoptosis and α-SMA/LC3 expression in the abdominal aortas. Protein levels were determined using western blotting.
resultsDEX administration repressed the dilation of aortas, alleviated pathological damage and cell apoptosis, and suppressed phenotype switching of vascular smooth muscle cells (VSMCs). Moreover, DEX activated autophagy and regulated the AMP-activated protein kinase/mammalian target of the rapamycin (AMPK/mTOR) signaling pathway in AAA rats. Administration of the AMPK inhibitor attenuated the DEX-mediated ameliorative effects on AAA in rats.
conclusionDEX ameliorates AAA in rat models by activating autophagy via the AMPK/mTOR pathway.
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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 OpenQuestion graph.