Mechanism and treatment of intracerebral hemorrhage focus on mitochondrial permeability transition pore

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2024-07-31 DOI:10.3389/fnmol.2024.1423132

Jing Cong, Jing-Yi Li, Wei Zou

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引用次数: 0

Abstract

Intracerebral hemorrhage (ICH) is the second most common subtype of stroke, characterized by high mortality and a poor prognosis. Despite various treatment methods, there has been limited improvement in the prognosis of ICH over the past decades. Therefore, it is imperative to identify a feasible treatment strategy for ICH. Mitochondria are organelles present in most eukaryotic cells and serve as the primary sites for aerobic respiration and energy production. Under unfavorable cellular conditions, mitochondria can induce changes in permeability through the opening of the mitochondrial permeability transition pore (mPTP), ultimately leading to mitochondrial dysfunction and contributing to various diseases. Recent studies have demonstrated that mPTP plays a role in the pathological processes associated with several neurodegenerative diseases including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, ischemic stroke and ischemia-reperfusion injury, among others. However, there is limited research on mPTP involvement specifically in ICH. Therefore, this study comprehensively examines the pathological processes associated with mPTP in terms of oxidative stress, apoptosis, necrosis, autophagy, ferroptosis, and other related mechanisms to elucidate the potential mechanism underlying mPTP involvement in ICH. This research aims to provide novel insights for the treatment of secondary injury after ICH.

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聚焦线粒体通透性转换孔的脑出血机制和治疗方法

脑内出血（ICH）是中风的第二大常见亚型，其特点是死亡率高、预后差。尽管有各种治疗方法，但过去几十年来，ICH 的预后改善有限。因此，当务之急是确定可行的 ICH 治疗策略。线粒体是存在于大多数真核细胞中的细胞器，是有氧呼吸和产生能量的主要场所。在不利的细胞条件下，线粒体可通过打开线粒体通透性转换孔（mPTP）引起通透性变化，最终导致线粒体功能障碍，引发各种疾病。最近的研究表明，mPTP 在与帕金森病、阿尔茨海默病、亨廷顿病、缺血性中风和缺血再灌注损伤等多种神经退行性疾病相关的病理过程中发挥作用。然而，专门针对 mPTP 参与 ICH 的研究还很有限。因此，本研究从氧化应激、细胞凋亡、坏死、自噬、铁蛋白沉积及其他相关机制等方面全面考察了与 mPTP 相关的病理过程，以阐明 mPTP 参与 ICH 的潜在机制。这项研究旨在为治疗 ICH 后的继发性损伤提供新的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.