泛视功能减退和自噬之间的相互作用:缺血性卒中的新疗法。

IF 3.5 3区 医学 Q2 NEUROSCIENCES
Frontiers in Molecular Neuroscience Pub Date : 2025-01-08 eCollection Date: 2024-01-01 DOI:10.3389/fnmol.2024.1482015
He-Yan Tian, Yun-Xing Lei, Jing-Tao Zhou, Long-Jun Liu, Tong Yang, Yue Zhou, Jin-Wen Ge, Chen Xu, Zhi-Gang Mei
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引用次数: 0

摘要

PANoptosis是一种新定义的程序性细胞死亡模式,涉及多种细胞死亡途径的激活,包括焦亡、凋亡和坏死亡,引发强烈的炎症反应。自噬是维持细胞稳态和保护细胞免受各种应激的重要细胞过程。脑缺血(IS)是一种由复杂的细胞死亡级联反应控制的脑部疾病,PANoptosis和自噬在其复杂的病理进展中都起着至关重要的作用,近年来它们之间潜在的相互作用引起了人们的关注。虽然越来越多的证据暗示IS中这两个过程之间存在相互作用,但潜在的机制仍然难以捉摸。因此,本文将深入探讨这种毁灭性疾病中PANoptosis和自噬相互作用的复杂机制。综上所述,IS中PANoptosis和自噬之间的串扰为开发新的卒中治疗方法提供了一个有希望的靶点。了解这两种途径之间的相互作用,为了解IS的潜在机制提供了急需的见解,并为新的治疗策略开辟了可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insight into interplay between PANoptosis and autophagy: novel therapeutics in ischemic stroke.

PANoptosis is a novelly defined mode of programmed cell death that involves the activation of multiple cellular death pathways, including pyroptosis, apoptosis, and necroptosis, triggering robust inflammatory reactions. Autophagy is a crucial cellular process that maintains cellular homeostasis and protects cells from various stresses. PANoptosis and autophagy, both vital players in the intricate pathological progression of ischemic stroke (IS), a brain ailment governed by intricate cell death cascades, have garnered attention in recent years for their potential interplay. While mounting evidence hints at a crosstalk between these two processes in IS, the underlying mechanisms remain elusive. Therefore, this review delves into and dissects the intricate mechanisms that underpin the intersection of PANoptosis and autophagy in this devastating condition. In conclusion, the crosstalk between PANoptosis and autophagy in IS presents a promising target for the development of novel stroke therapies. Understanding the interplay between these two pathways offers a much-needed insight into the underlying mechanisms of IS and opens the possibility for new therapeutic strategies.

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来源期刊
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.
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