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调节性细胞死亡的机制:由特定蛋白质诱导或抑制的结构和功能蛋白质组学途径——综述

The Mechanisms of Regulated Cell Death: Structural and Functional Proteomic Pathways Induced or Inhibited by a Specific Protein-A Narrative Review.

作者信息

Fernández-Lázaro Diego, Sanz Begoña, Seco-Calvo Jesús

机构信息

Department of Cellular Biology, Genetics, Histology and Pharmacology, Faculty of Health Sciences, University of Valladolid, Campus of Soria, 42004 Soria, Spain.

Neurobiology Research Group, Faculty of Medicine, University of Valladolid, 47005 Valladolid, Spain.

出版信息

Proteomes. 2024 Jan 5;12(1):3. doi: 10.3390/proteomes12010003.

Abstract

Billions of cells die in us every hour, and our tissues do not shrink because there is a natural regulation where Cell Death (CD) is balanced with cell division. The process in which cells eliminate themselves in a controlled manner is called Programmed Cell Death (PCD). The PCD plays an important role during embryonic development, in maintaining homeostasis of the body's tissues, and in the elimination of damaged cells, under a wide range of physiological and developmental stimuli. A multitude of protein mediators of PCD have been identified and signals have been found to utilize common pathways elucidating the proteins involved. This narrative review focuses on caspase-dependent and caspase-independent PCD pathways. Included are studies of caspase-dependent PCD such as Anoikis, Catastrophe Mitotic, Pyroptosis, Emperitosis, Parthanatos and Cornification, and Caspase-Independent PCD as Wallerian Degeneration, Ferroptosis, Paraptosis, Entosis, Methuosis, and Extracellular Trap Abnormal Condition (ETosis), as well as neutrophil extracellular trap abnormal condition (NETosis) and Eosinophil Extracellular Trap Abnormal Condition (EETosis). Understanding PCD from those reported in this review could shed substantial light on the processes of biological homeostasis. In addition, identifying specific proteins involved in these processes is mandatory to identify molecular biomarkers, as well as therapeutic targets. This knowledge could provide the ability to modulate the PCD response and could lead to new therapeutic interventions in a wide range of diseases.

摘要

我们体内每小时都有数十亿细胞死亡,但我们的组织不会萎缩,因为存在一种自然调节机制,即细胞死亡(CD)与细胞分裂保持平衡。细胞以可控方式自我清除的过程称为程序性细胞死亡(PCD)。在胚胎发育过程中、维持身体组织的内环境稳定以及在各种生理和发育刺激下清除受损细胞的过程中,PCD都起着重要作用。已经鉴定出多种PCD的蛋白质介质,并且发现信号利用共同途径来阐明所涉及的蛋白质。这篇叙述性综述重点关注半胱天冬酶依赖性和半胱天冬酶非依赖性PCD途径。其中包括对半胱天冬酶依赖性PCD的研究,如失巢凋亡、有丝分裂灾难、焦亡、穿孔素介导的细胞死亡、PARP-1依赖性细胞坏死和角质化,以及半胱天冬酶非依赖性PCD,如沃勒变性、铁死亡、Paraptosis、细胞内吞、Methuosis和细胞外陷阱异常状态(ETosis),以及中性粒细胞胞外陷阱异常状态(NETosis)和嗜酸性粒细胞胞外陷阱异常状态(EETosis)。从本综述中报道的这些方面了解PCD,可能会为生物稳态过程提供大量启示。此外,识别参与这些过程的特定蛋白质对于识别分子生物标志物以及治疗靶点至关重要。这些知识可以提供调节PCD反应的能力,并可能导致对多种疾病的新治疗干预。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f494/10801515/c17b229ce1ad/proteomes-12-00003-g001.jpg

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