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功能失调的能量以及低剂量羟基酪醇作为神经退行性疾病保护剂的未来前景。

Dysfunctional energy and future perspective of low dose HO as protective agent in neurodegenerative disease.

作者信息

Widyarti Sri, Wibowo Syahputra, Sabarudin Akhmad, Abhirama Intan, Sumitro Sutiman Bambang

机构信息

Department of Biology, Faculty of Mathematics and Natural Sciences, Brawijaya University, Jl. Veteran, Malang 65145, East Java, Indonesia.

Postdoctoral Fellow, Faculty of Biology, Gadjah Mada University, Teknika Selatan Sekip Utara, 55281 Yogyakarta, Indonesia.

出版信息

Heliyon. 2023 Jul 16;9(7):e18123. doi: 10.1016/j.heliyon.2023.e18123. eCollection 2023 Jul.

Abstract

The number of people with neurodegenerative disease continues to increase every year. A new perspective is needed to overcome this disease. In this review, researchers collected information about dysfunctional energy in neurodegenerative diseases driven by mitochondria. Mitochondrial dysregulation can cause damage to the neuron system. The increase in the amount and interaction of α-synuclein with SAMM50 and GABARAPL1 in the mitochondria is one of the factors causing neurodegenerative disease. As an energy provider in the body, the existence of harmonization in the regulation of mitochondria, specifically the mitochondrial outer membrane, is important. Low-dose hydrogen peroxide (HO) has neuroprotective abilities to overcome the impairment function of mitochondria in neurodegenerative patients. Based on computational simulation of this case, it can be used as a basic concept for the development of the role of HO in neurodegenerative diseases.

摘要

神经退行性疾病患者的数量每年都在持续增加。需要一种新的视角来攻克这种疾病。在这篇综述中,研究人员收集了有关线粒体驱动的神经退行性疾病中能量功能失调的信息。线粒体功能失调会导致神经系统受损。线粒体中α-突触核蛋白与SAMM50和GABARAPL1的数量增加及相互作用是导致神经退行性疾病的因素之一。作为身体中的能量供应者,线粒体,特别是线粒体外膜的调节中存在协调作用很重要。低剂量过氧化氢(HO)具有神经保护能力,可克服神经退行性疾病患者线粒体的功能损伤。基于此案例的计算模拟,它可作为开发HO在神经退行性疾病中作用的基本概念。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c7f/10372669/3e720acff455/gr1.jpg

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