姜黄素在自噬调节中的治疗潜力:对转录因子 EB 作用的见解

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Shabnam Radbakhsh , Prashant Kesharwani , Amirhossein Sahebkar
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引用次数: 0

摘要

转录因子 EB(TFEB)是基本螺旋-环-螺旋/亮氨酸拉链(bHLHZip)类 DNA 结合蛋白,可控制自噬-溶酶体途径中基因的表达。TFEB 通过增强溶酶体的生物生成、形成自噬体以及与溶酶体融合来调节自噬通量,从而促进细胞对致病蛋白结构的清除。姜黄素是一种天然多酚分子,其药理特性使其成为治疗多种疾病的潜在候选药物。姜黄素的重要作用机制之一包括通过影响各种信号成分(如 TFEB)来调节自噬。本综述将讨论姜黄素通过调节 TFEB 的活性对不同疾病的自噬过程产生影响的体外和体内证据。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Therapeutic potential of curcumin in autophagy modulation: Insights into the role of transcription factor EB

Transcription factor EB (TFEB) is a basic Helix–Loop–Helix/Leucine Zipper (bHLHZip) class of DNA-binding proteins, which can control the expression of genes included in the autophagy–lysosomal pathway. TFEB regulates the autophagic flux by enhancing lysosome biogenesis, forming autophagosomes, and fusion with lysosomes, thereby facilitating cellular clearance of pathogenic protein structures. Curcumin is a natural polyphenolic molecule with pharmacological properties that make it a potential therapeutic candidate for a wide range of diseases. One of the important curcumin mechanisms of action includes modulation of autophagy through affecting various signaling components such as TFEB. This review discusses in vitro and in vivo evidence on the effects of curcumin on autophagy process via modulating TFEB activity in different disorders.

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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
24
审稿时长
51 days
期刊介绍: Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.
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