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探索骨骼肌中IGF-1通过甲状腺激素-自噬信号通路对DUOX的潜在调控(综述)

Exploring the potential regulation of DUOX in thyroid hormone‑autophagy signaling via IGF‑1 in the skeletal muscle (Review).

作者信息

Then Andreas Adiwinata, Goenawan Hanna, Lesmana Ronny, Christoper Andreas, Sylviana Nova, Gunadi Julia Windi

机构信息

Master's Program in Basic Biomedical Sciences, Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Bandung, West Java 40161, Indonesia.

Department of Biomedical Sciences, Faculty of Medicine, Universitas Padjadjaran, Jatinangor-Sumedang, West Java 45363, Indonesia.

出版信息

Biomed Rep. 2024 Dec 24;22(3):39. doi: 10.3892/br.2024.1917. eCollection 2025 Mar.

DOI:10.3892/br.2024.1917
PMID:39781041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11704872/
Abstract

Dual oxidases (DUOX) are enzymes that have the main function in producing reactive oxygen species (ROS) in various tissues. DUOX also play an important role in the synthesis of HO, which is essential for the production of thyroid hormone. Thyroid hormones can influence the process of muscle development through direct stimulation of ROS, 5' AMP-activated protein kinase (AMPK) and mTOR and indirect effect autophagy and the insulin-like growth factor 1 (IGF-1) pathway. IGF-1 signaling controls autophagy in two ways: Inhibiting autophagy through activation of the PI3K/AKT/mTOR/MAPK pathway and promoting mitophagy through the nuclear factor erythroid 2-related factor 2-binding receptor Bcl2/adenovirus E1B 19 kDa protein-interacting protein 3. Thyroid hormone deficiency caused by the absence of DUOX should be considered because it might have a significant effect on the growth of skeletal muscle. The effect of DUOX regulation on thyroid hormone autophagy via IGF-1 in skeletal muscle has not been well investigated. The present review discussed the regulatory interactions between DUOX, thyroid hormone, IGF-1 and autophagy, which can influence skeletal muscle development.

摘要

双氧化酶(DUOX)是一类在多种组织中主要负责产生活性氧(ROS)的酶。DUOX在过氧化氢(HO)的合成中也发挥着重要作用,而过氧化氢对于甲状腺激素的产生至关重要。甲状腺激素可通过直接刺激ROS、5'-腺苷酸活化蛋白激酶(AMPK)和雷帕霉素靶蛋白(mTOR)以及间接影响自噬和胰岛素样生长因子1(IGF-1)信号通路来影响肌肉发育过程。IGF-1信号通路通过两种方式控制自噬:通过激活磷脂酰肌醇-3激酶(PI3K)/蛋白激酶B(AKT)/mTOR/丝裂原活化蛋白激酶(MAPK)通路抑制自噬,以及通过核因子E2相关因子2结合受体Bcl2/腺病毒E1B 19 kDa蛋白相互作用蛋白3促进线粒体自噬。应考虑由DUOX缺失导致的甲状腺激素缺乏,因为它可能对骨骼肌生长产生重大影响。DUOX调节通过IGF-1对骨骼肌中甲状腺激素自噬的影响尚未得到充分研究。本综述讨论了DUOX、甲状腺激素、IGF-1和自噬之间的调节相互作用,这些相互作用会影响骨骼肌发育。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/008cc94ea9fa/br-22-03-01917-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/877429f3ec57/br-22-03-01917-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/c00b0c0b99ee/br-22-03-01917-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/bbb69d6bf002/br-22-03-01917-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/e7f6e0320259/br-22-03-01917-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/008cc94ea9fa/br-22-03-01917-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/877429f3ec57/br-22-03-01917-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/c00b0c0b99ee/br-22-03-01917-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/bbb69d6bf002/br-22-03-01917-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/e7f6e0320259/br-22-03-01917-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e853/11704872/008cc94ea9fa/br-22-03-01917-g04.jpg

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