{"title":"Therapeutic potential of curcumin in autophagy modulation: Insights into the role of transcription factor EB","authors":"Shabnam Radbakhsh , Prashant Kesharwani , Amirhossein Sahebkar","doi":"10.1016/j.mrfmmm.2024.111879","DOIUrl":null,"url":null,"abstract":"<div><p>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 <em>in vitro</em> and <em>in vivo</em> evidence on the effects of curcumin on autophagy process <em>via</em> modulating TFEB activity in different disorders.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111879"},"PeriodicalIF":1.5000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0027510724000290","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
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.
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.