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- W4386898488 abstract "Aortic dissection (AD) presents a medical challenge for clinicians. Here, to determine the role of a novel small non-coding piRNA-823 (piR-823) in AD, murine and human aorta from patients with AD were used. A high expression levels of piR-823 were found in patients with AD. Using performed loss- and gain-of-function assays in vitro and in vivo, we explore the regulatory effect of piR-823 on vascular smooth muscle cells (VSMCs) and AD. piR-823 obviously facilitates the proliferation, migration, and phenotypic transformation of VSMCs with or without nicotine treatment. piR-823 directly binds and suppresses histone deacetylase 1 (HDAC1) expression, and regulates the acetylation of histone 3 (H3) via H3K9ac and H3K27ac, eventually, VSMC functions and AD. To consolidate our findings, AD murine model was performed, and we observed that piR-823 antagomir strongly inhibited the pathogenesis of AD through regulating vascular remodeling. Thus, our study finds a potential target for the prevention and treatment strategy for nicotine-induced AD." @default.
- W4386898488 created "2023-09-21" @default.
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- W4386898488 date "2023-10-01" @default.
- W4386898488 modified "2023-10-05" @default.
- W4386898488 title "piRNA-823 is a Novel Potential Therapeutic Target in Aortic Dissection" @default.
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- W4386898488 doi "https://doi.org/10.1016/j.phrs.2023.106932" @default.
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