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已发表论文
阿尔茨海默病发病机制中线粒体炎症调节的理解进展
Authors Zhang RZ, Li L, Ma C, Dou TT, Wei YT, Yan XK
Received 29 July 2025
Accepted for publication 8 October 2025
Published 23 October 2025 Volume 2025:18 Pages 14475—14491
DOI https://doi.org/10.2147/JIR.S557000
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Prof. Dr. Dharmappa Krishnappa
Ren-Zhen Zhang,1,* Li Li,1,* Cui Ma,1 Ting-Ting Dou,1 Yu-Ting Wei,1 Xing-Ke Yan1,2
1School of Acupuncture-Moxibustion and Tuina, Gansu University of Traditional Chinese Medicine, Lanzhou, People’s Republic of China; 2Gansu Provincial Traditional Chinese Medicine Research Center, Lanzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xing-Ke Yan, Acupuncture and moxibustion and Massage College of Gansu University of Traditional Chinese Medicine, 35 Dingxi East Road, Lanzhou, People’s Republic of China, Email yanxingke@126.com
Abstract: Mitochondria, beyond serving as the powerhouse of the cell, play a pivotal role in the regulation of inflammatory responses. Mitochondrial dysfunction-induced immune activation and chronic inflammation are deeply implicated in the pathogenesis of Alzheimer’s disease (AD), influencing its onset and progression through multiple inflammatory pathways. This review summarizes the involvement of several mitochondrial-related mechanisms in AD, including the release of mitochondrial DNA (mtDNA), signal transduction via mitochondrial antiviral-signaling protein (MAVS), the accumulation of mitochondrial damage-associated molecular patterns (DAMPs), the regulation of mitophagy, and the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. These insights aim to shed new light on mitochondrial inflammation as a regulatory mechanism in AD and to explore its potential as a therapeutic target.
Keywords: Alzheimer’s disease, mitochondrion, neuroinflammation, inflammatory mechanism, review
1School of Acupuncture-Moxibustion and Tuina, Gansu University of Traditional Chinese Medicine, Lanzhou, People’s Republic of China; 2Gansu Provincial Traditional Chinese Medicine Research Center, Lanzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Xing-Ke Yan, Acupuncture and moxibustion and Massage College of Gansu University of Traditional Chinese Medicine, 35 Dingxi East Road, Lanzhou, People’s Republic of China, Email yanxingke@126.com
Abstract: Mitochondria, beyond serving as the powerhouse of the cell, play a pivotal role in the regulation of inflammatory responses. Mitochondrial dysfunction-induced immune activation and chronic inflammation are deeply implicated in the pathogenesis of Alzheimer’s disease (AD), influencing its onset and progression through multiple inflammatory pathways. This review summarizes the involvement of several mitochondrial-related mechanisms in AD, including the release of mitochondrial DNA (mtDNA), signal transduction via mitochondrial antiviral-signaling protein (MAVS), the accumulation of mitochondrial damage-associated molecular patterns (DAMPs), the regulation of mitophagy, and the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway. These insights aim to shed new light on mitochondrial inflammation as a regulatory mechanism in AD and to explore its potential as a therapeutic target.
Keywords: Alzheimer’s disease, mitochondrion, neuroinflammation, inflammatory mechanism, review