自噬损伤介导尿酸诱导的血管平滑肌细胞表型转化。

IF 2.9 4区 医学 Q2 PHARMACOLOGY & PHARMACY
Pharmacology Pub Date : 2024-01-01 Epub Date: 2023-11-27 DOI:10.1159/000534929
Yan Lu, Hanlin Zhang, Min Han, Ping Wang, Liping Meng
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引用次数: 0

摘要

导读:高尿酸血症可能参与血管平滑肌细胞的表型转化,从而促进动脉粥样硬化的发生,自噬可能是其中的重要环节之一,但具体的分子机制尚不清楚。方法:建立小鼠高尿酸血症模型,研究自噬水平变化与肌肉细胞表型转化的关系。结果:我们的研究发现,高尿酸水平通过抑制自噬促进肌肉细胞的表型转化,从而增强肌肉细胞的增殖和迁移能力。如果自噬恢复,表型转化可以通过降低转录因子kruppel样因子4的水平来逆转。结论:尿酸可能通过破坏肌细胞正常自噬,诱导肌细胞表型转化,促进动脉粥样硬化的发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Impairment of Autophagy Mediates the Uric-Acid-Induced Phenotypic Transformation of Vascular Smooth Muscle Cells.

Introduction: Hyperuricemia may be involved in the phenotypic transformation of vascular smooth muscle cells, thus promoting the occurrence of atherosclerosis, and autophagy may be one of the important links, but little is known about the specific molecular mechanism.

Methods: We established a mouse model of hyperuricemia and studied the relationship between changes in autophagy levels and the phenotypic transformation of muscle cells.

Results: Our study found that high uric acid levels promote the phenotypic transformation of muscle cells by inhibiting autophagy, thus enhancing their proliferation and migration abilities. If autophagy is restored, phenotypic transformation can be reversed by reducing the levels of the transcription factor Kruppel-like factor 4.

Conclusion: Uric acid may induce the phenotypic transformation of muscle cells and promote the occurrence of atherosclerosis by disrupting normal autophagy.

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来源期刊
Pharmacology
Pharmacology 医学-药学
CiteScore
5.60
自引率
0.00%
发文量
52
审稿时长
6-12 weeks
期刊介绍: ''Pharmacology'' is an international forum to present and discuss current perspectives in drug research. The journal communicates research in basic and clinical pharmacology and related fields. It covers biochemical pharmacology, molecular pharmacology, immunopharmacology, drug metabolism, pharmacogenetics, analytical toxicology, neuropsychopharmacology, pharmacokinetics and clinical pharmacology. In addition to original papers and short communications of investigative findings and pharmacological profiles the journal contains reviews, comments and perspective notes; research communications of novel therapeutic agents are encouraged.
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