Endoplasmic reticulum stress and autophagy in HIV-1-associated neurocognitive disorders
Endoplasmic reticulum stress and autophagy in HIV-1-associated neurocognitive disorders
复制标题
HIV-1相关神经认知障碍中的内质网应激和自噬
DOI：
10.1007/s13365-020-00906-4
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发表时间：
2020-09
影响因子：
3.2
通讯作者：
Yulin Zhang
中科院分区：
文献类型：
--
作者：
Xue Chen;Tong Zhang;Yulin Zhang
虽然抗逆转录病毒治疗（ART）影响病毒抑制和预期寿命的艾滋病毒阳性患者;艾滋病毒-1相关的神经认知障碍（HAND）继续诊断艾滋病毒-1患者正在接受治疗。HAND广泛的临床表现包括行为、认知和运动功能障碍，严重影响患者的生活质量。HAND的发病机制作为改善其治疗的潜在途径已受到越来越多的关注。大量研究表明，内质网应激、自噬及其相互作用在神经退行性疾病的发生、发展中起着重要作用。虽然错误折叠蛋白的积累可以诱导ER应激，但自噬可以有效地清除积累的毒性蛋白，减轻ER应激，从而抑制神经病变的发展。通过对内质网应激和自噬的深入研究，两者都被认为是药物干预治疗HAND的有希望的靶点。这篇综述将突出ER应激、自噬及其在HAND背景下的相互作用的影响，从而有助于为HAND患者的靶向治疗的未来发展提供信息。
Although antiretroviral therapy (ART) affects virologic suppression and prolongs life expectancies among HIV-positive patients; HIV-1-associated neurocognitive disorders (HAND) continue to be diagnosed in patients with HIV-1 undergoing treatment. The extensive clinical manifestations of HAND include behavioral, cognitive, and motor dysfunctions that severely affect the patients’ quality of life. The pathogenesis of HAND has received increasing attention as a potential avenue by which to improve the treatment of the condition. Many studies have shown that endoplasmic reticulum (ER) stress, autophagy, and their interaction play important roles in the onset and development of neurodegenerative diseases. While the accumulation of misfolded proteins can induce ER stress, autophagy can effectively remove accumulated toxic proteins, reduce ER stress, and thus inhibit the development of neuropathy. Through the in-depth study of ER stress and autophagy, both have been recognized as promising targets for pharmacotherapeutic intervention in the treatment of HAND. This review will highlight the effects of ER stress, autophagy, and their interaction in the context of HAND, thereby helping to inform the future development of targeted treatments for patients with HAND.
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DOI：
10.1093/brain/aws143
发表时间：
2012-07
期刊：
Brain : a journal of neurology
影响因子：
--
作者：
Schaeffer V;Lavenir I;Ozcelik S;Tolnay M;Winkler DT;Goedert M
通讯作者：
Goedert M
影响因子：
12.7
作者：
Scheper W;Hoozemans JJ
通讯作者：
Hoozemans JJ
影响因子：
28.2
作者：
Karsli-Uzunbas G;Guo JY;Price S;Teng X;Laddha SV;Khor S;Kalaany NY;Jacks T;Chan CS;Rabinowitz JD;White E
通讯作者：
White E
影响因子：
21.3
作者：
Tabas, Ira;Ron, David
通讯作者：
Ron, David
影响因子：
2.5
作者：
Cheryl Ligon;Yu Cai;S. Buch;J. Arikkath
通讯作者：
Cheryl Ligon;Yu Cai;S. Buch;J. Arikkath