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SIRT3参与调节自噬相关机制的研究进展。

Advances in SIRT3 involvement in regulating autophagy-related mechanisms.

作者信息

Xi Shuangyun, Chen Weijun, Ke Yong

机构信息

Center of Forensic Expertise, Affiliated hospital of Zunyi Medical University, Zunyi, 563000, Guizhou, China.

School of Forensic Medicine, Zunyi Medical University, Zunyi, 563000, Guizhou, China.

出版信息

Cell Div. 2024 Jun 12;19(1):20. doi: 10.1186/s13008-024-00124-y.

Abstract

The silencing regulatory factor 2-like protein 3 (SIRT3) is a nicotinamide adenine dinucleotide (NAD+) dependent deacetylase located primarily in the mitochondria. This protein plays an important role in oxidative stress, energy metabolism, and autophagy in multicellular organisms. Autophagy (macroautophagy) is primarily a cytoprotective mechanism necessary for intracellular homeostasis and the synthesis, degradation, and recycling of cellular products. Autophagy can influence the progression of several neural, cardiac, hepatic, and renal diseases and can also contribute to the development of fibrosis, diabetes, and many types of cancer. Recent studies have shown that SIRT3 has an important role in regulating autophagy. Therefore in this study, we aimed to perform a literature review to summarize the role of SIRT3 in the regulation of cellular autophagy. The findings of this study could be used to identify new drug targets for SIRT3-related diseases. Methods: A comprehensive literature review of the mechanism involved behind SIRT3 and autophagy-related diseases was performed. Relevant literature published in Pubmed and Web of Science up to July 2023 was identified using the keywords "silencing regulatory factor 2-like protein 3", "SIRT3" and "autophagy".

摘要

沉默调节因子2样蛋白3(SIRT3)是一种主要位于线粒体的烟酰胺腺嘌呤二核苷酸(NAD+)依赖性脱乙酰酶。该蛋白在多细胞生物的氧化应激、能量代谢和自噬中发挥重要作用。自噬(巨自噬)主要是一种细胞保护机制,对细胞内稳态以及细胞产物的合成、降解和循环至关重要。自噬可影响多种神经、心脏、肝脏和肾脏疾病的进展,也可促进纤维化、糖尿病和多种癌症的发展。最近的研究表明,SIRT3在调节自噬中起重要作用。因此,在本研究中,我们旨在进行文献综述,总结SIRT3在调节细胞自噬中的作用。本研究的结果可用于确定SIRT3相关疾病的新药物靶点。方法:对SIRT3与自噬相关疾病背后的机制进行了全面的文献综述。使用关键词“沉默调节因子2样蛋白3”、“SIRT3”和“自噬”,检索了截至2023年7月发表在PubMed和Web of Science上的相关文献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ce1/11170824/b66cd2ea2df9/13008_2024_124_Fig1_HTML.jpg

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