ArticleZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences2019
[Autophagy regulates the function of vascular smooth muscle cells in the formation and rupture of intracranial aneurysms].
Article in Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Exploring the roles and therapeutic implications of melatonin-mediated KLF6 in the development of intracranial aneurysm.Annals of medicine · 2024Article
- ADORA3: A Key Player in the Pathogenesis of Intracranial Aneurysms and a Potential Diagnostic Biomarker.Molecular diagnosis & therapy · 2024Article
- Comprehensive Analysis of Endoplasmic Reticulum Stress in Intracranial Aneurysm.Frontiers in cellular neuroscience · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Vascular smooth muscle cells (VSMC) are the main cellular component of vessel wall. The changes of VSMC functions including phenotypic transformation and apoptosis play a critical role in the pathogenesis of intracranial aneurysm (IA). Autophagy can participate in the regulation of vascular function by regulating cell function. In the initial stage of IA, the activation of autophagy can accelerate the phenotypic transformation of VSMC and inhibit VSMC apoptosis. With the progress of IA, the relationship between autophagy and apoptosis changes from antagonism to synergy or promotion, and a large number of apoptotic VSMC lead to the rupture of IA. In this review, we describe the role of autophagy regulating the function of VSMC in the occurrence, development and rupture of IA, for further understanding the pathogenesis of IA and finding molecular targets to prevent the formation and rupture of IA.
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Registered trials
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