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Role of exosome-associated microRNA in diagnostic and therapeutic applications to metabolic disorders / 浙江大学学报(英文版)(B辑:生物医学和生物技术)
Article in En | WPRIM | ID: wpr-1010379
Responsible library: WPRO
ABSTRACT
Metabolic disorders are classified clinically as a complex and varied group of diseases including metabolic syndrome, obesity, and diabetes mellitus. Fat toxicity, chronic inflammation, and oxidative stress, which may change cellular functions, are considered to play an essential role in the pathogenetic progress of metabolic disorders. Recent studies have found that cells secrete nanoscale vesicles containing proteins, lipids, nucleic acids, and membrane receptors, which mediate signal transduction and material transport to neighboring and distant cells. Exosomes, one type of such vesicles, are reported to participate in multiple pathological processes including tumor metastasis, atherosclerosis, chronic inflammation, and insulin resistance. Research on exosomes has focused mainly on the proteins they contain, but recently the function of exosome-associated microRNA has drawn a lot of attention. Exosome-associated microRNAs regulate the physiological function and pathological processes of metabolic disorders. They may also be useful as novel diagnostics and therapeutics given their special features of non-immunogenicity and quick extraction. In this paper, we summarize the structure, content, and functions of exosomes and the potential diagnostic and therapeutic applications of exosome-associated microRNAs in the treatment of metabolic disorders.
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Full text: 1 Database: WPRIM Main subject: Adipose Tissue / MicroRNAs / Exosomes / Tumor Microenvironment / Metabolic Diseases Limits: Animals / Humans Language: En Journal: Journal of Zhejiang University. Science. B Year: 2018 Document type: Article
Full text: 1 Database: WPRIM Main subject: Adipose Tissue / MicroRNAs / Exosomes / Tumor Microenvironment / Metabolic Diseases Limits: Animals / Humans Language: En Journal: Journal of Zhejiang University. Science. B Year: 2018 Document type: Article