ArticleAmerican journal of translational research2019
HSP90 inhibitor 17-DMAG effectively alleviated the progress of thoracic aortic dissection by suppressing smooth muscle cell phenotypic switch.
Article in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Comprehensive analysis of the lncRNA-miRNA-mRNA ceRNA network in aortic dissection.Archives of medical science : AMS · 2026Article
- Aspirin relieves the calcification of aortic smooth muscle cells by enhancing the heat shock response.Pharmaceutical biology · 2022Article
- The role of vascular smooth muscle cells in the development of aortic aneurysms and dissections.European journal of clinical investigation · 2022Review
- Assessing serum levels of SM22α as a new biomarker for patients with aortic aneurysm/dissection.PloS one · 2022Article
- Dysregulated long non-coding RNAs involved in regulation of matrix degradation during type-B aortic dissection pathogenesis.General thoracic and cardiovascular surgery · 2021Article
- Differentially Expressed Long Noncoding RNAs Involved in FUBP1 Promoting Hepatocellular Carcinoma Cells Proliferation.BioMed research international · 2021Article
- Heat shock protein 90 inhibitor AUY922 attenuates platelet-derived growth factor-BB-induced migration and proliferation of vascular smooth muscle cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- Integration of Gene Expression Profile Data to Verify Hub Genes of Patients with Stanford A Aortic Dissection.BioMed research international · 2019Article
- Article
- Induction of thoracic aortic dissection: a mini-review of β-aminopropionitrile-related mouse models.Journal of Zhejiang University. Science. BReview
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thoracic aortic dissection (TAD) is a highly lethal vascular disease characterized by medial degeneration. Heat shock protein 90 (HSP90) had been proved as a potential target for a variety of diseases. The aim of this study was to identify the effect of HSP90 inhibitor on TAD progress, and to explore the potential utility of HSP90 inhibitors as therapeutic avenue for TAD. In clinical samples, the elevated HSP90 expression was detected in aortic walls from TAD patients (n=20) by real-time PCR and western blot, and was positively correlated with osteopontin (OPN), a synthetic phenotypic marker of smooth muscle cells (SMCs), while negatively correlated with SM22, a contractile phenotypic marker. In a β-aminopropionitrile fumarate-induced AD mice model, 17-DMAG, a HSP90-inhibitor, effectively reduced the incidence and mortality of TAD. Histological examination confirmed that 17-DMAG significantly alleviated the loss of elastic fibers integrity. Meanwhile, the phenotypic switch of SMCs was significantly suppressed by 17-DMAG, demonstrated by the change of phenotypic markers expression. On the cellular level, 17-DMAG suppressed phenotypic switch of SMCs induced by PDGF-bb, and significantly depressed the excessive proliferation and migration of SMCs. Flow cytometry analysis showed that 17-DMAG induced cell cycle arrest in G1 phase. In summary, 17-DMAG could effectively alleviate the TAD progress by suppressing SMCs phenotypic switch, and inhibition of HSP90 might be a potential avenue for TAD therapy.
Indexed as
Identifiers
30788006PMC6357309W2994605618What OpenQuestion holds
Registered trials
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