首页 > 最新文献

Trends in Cell Biology最新文献

英文 中文
The epitranscriptome: reshaping the DNA damage response. 表转录组:重塑 DNA 损伤反应。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-23 DOI: 10.1016/j.tcb.2024.06.008
Vivian Kalamara, George A Garinis

Genomic instability poses a formidable threat to cellular vitality and wellbeing, prompting cells to deploy an intricate DNA damage response (DDR) mechanism. Recent evidence has suggested that RNA is intricately linked to the DDR by serving as template, scaffold, or regulator during the repair of DNA damage. Additionally, RNA molecules undergo modifications, contributing to the epitranscriptome, a dynamic regulatory layer influencing cellular responses to genotoxic stress. The intricate interplay between RNA and the DDR sheds new light on how the RNA epigenome contributes to the maintenance of genomic integrity and ultimately shapes the fate of damaged cells.

基因组的不稳定性对细胞的活力和健康构成了巨大威胁,促使细胞部署复杂的 DNA 损伤应答(DDR)机制。最近的证据表明,RNA 在 DNA 损伤修复过程中充当模板、支架或调节器的角色,与 DDR 密切相关。此外,RNA 分子会发生修饰,从而形成表转录组(epitranscriptome),这是一个影响细胞对基因毒性应激反应的动态调控层。RNA 与 DDR 之间错综复杂的相互作用为我们揭示了 RNA 表观基因组如何有助于维持基因组完整性并最终决定受损细胞的命运。
{"title":"The epitranscriptome: reshaping the DNA damage response.","authors":"Vivian Kalamara, George A Garinis","doi":"10.1016/j.tcb.2024.06.008","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.06.008","url":null,"abstract":"<p><p>Genomic instability poses a formidable threat to cellular vitality and wellbeing, prompting cells to deploy an intricate DNA damage response (DDR) mechanism. Recent evidence has suggested that RNA is intricately linked to the DDR by serving as template, scaffold, or regulator during the repair of DNA damage. Additionally, RNA molecules undergo modifications, contributing to the epitranscriptome, a dynamic regulatory layer influencing cellular responses to genotoxic stress. The intricate interplay between RNA and the DDR sheds new light on how the RNA epigenome contributes to the maintenance of genomic integrity and ultimately shapes the fate of damaged cells.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ADAR1: from basic mechanisms to inhibitors. ADAR1:从基本机制到抑制剂。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-18 DOI: 10.1016/j.tcb.2024.06.006
Jan Rehwinkel, Parinaz Mehdipour

Adenosine deaminase acting on RNA 1 (ADAR1) converts adenosine to inosine in double-stranded RNA (dsRNA) molecules, a process known as A-to-I editing. ADAR1 deficiency in humans and mice results in profound inflammatory diseases characterised by the spontaneous induction of innate immunity. In cells lacking ADAR1, unedited RNAs activate RNA sensors. These include melanoma differentiation-associated gene 5 (MDA5) that induces the expression of cytokines, particularly type I interferons (IFNs), protein kinase R (PKR), oligoadenylate synthase (OAS), and Z-DNA/RNA binding protein 1 (ZBP1). Immunogenic RNAs 'defused' by ADAR1 may include transcripts from repetitive elements and other long duplex RNAs. Here, we review these recent fundamental discoveries and discuss implications for human diseases. Some tumours depend on ADAR1 to escape immune surveillance, opening the possibility of unleashing anticancer therapies with ADAR1 inhibitors.

作用于 RNA 的腺苷脱氨酶 1(ADAR1)可将双链 RNA(dsRNA)分子中的腺苷转化为肌苷,这一过程被称为 "A-to-I 编辑"。人类和小鼠缺乏 ADAR1 会导致以自发诱导先天性免疫为特征的严重炎症性疾病。在缺乏 ADAR1 的细胞中,未经编辑的 RNA 会激活 RNA 传感器。其中包括黑色素瘤分化相关基因 5(MDA5),它能诱导细胞因子(尤其是 I 型干扰素(IFN))、蛋白激酶 R(PKR)、寡腺苷酸合成酶(OAS)和 Z-DNA/RNA 结合蛋白 1(ZBP1)的表达。被 ADAR1 "化解 "的免疫原性 RNA 可能包括来自重复元件和其他长双链 RNA 的转录本。在此,我们回顾了这些最新的基本发现,并讨论了它们对人类疾病的影响。一些肿瘤依赖 ADAR1 逃避免疫监视,这为利用 ADAR1 抑制剂释放抗癌疗法提供了可能。
{"title":"ADAR1: from basic mechanisms to inhibitors.","authors":"Jan Rehwinkel, Parinaz Mehdipour","doi":"10.1016/j.tcb.2024.06.006","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.06.006","url":null,"abstract":"<p><p>Adenosine deaminase acting on RNA 1 (ADAR1) converts adenosine to inosine in double-stranded RNA (dsRNA) molecules, a process known as A-to-I editing. ADAR1 deficiency in humans and mice results in profound inflammatory diseases characterised by the spontaneous induction of innate immunity. In cells lacking ADAR1, unedited RNAs activate RNA sensors. These include melanoma differentiation-associated gene 5 (MDA5) that induces the expression of cytokines, particularly type I interferons (IFNs), protein kinase R (PKR), oligoadenylate synthase (OAS), and Z-DNA/RNA binding protein 1 (ZBP1). Immunogenic RNAs 'defused' by ADAR1 may include transcripts from repetitive elements and other long duplex RNAs. Here, we review these recent fundamental discoveries and discuss implications for human diseases. Some tumours depend on ADAR1 to escape immune surveillance, opening the possibility of unleashing anticancer therapies with ADAR1 inhibitors.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141728381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Immune surveillance of senescence: potential application to age-related diseases 衰老的免疫监视:在老年相关疾病中的潜在应用
IF 19 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-17 DOI: 10.1016/j.tcb.2024.06.007

Several lines of evidence suggest that the age-dependent accumulation of senescent cells leads to chronic tissue microinflammation, which in turn contributes to age-related pathologies. In general, senescent cells can be eliminated by the host’s innate and adaptive immune surveillance system, including macrophages, NK cells, and T cells. Impaired immune surveillance leads to the accumulation of senescent cells and accelerates the aging process. Recently, senescent cells, like cancer cells, have been shown to express certain types of immune checkpoint proteins as well as non-classical immune-tolerant MHC variants, leading to immune escape from surveillance systems. Thus, immune checkpoint blockade (ICB) may be a promising strategy to enhance immune surveillance of senescence, leading to the amelioration of some age-related diseases and tissue dysfunction.

多种证据表明,衰老细胞的积累与年龄有关,会导致慢性组织微炎症,进而引发与年龄有关的病症。一般来说,衰老细胞可被宿主的先天性和适应性免疫监视系统(包括巨噬细胞、NK 细胞和 T 细胞)清除。免疫监视功能受损会导致衰老细胞的积累并加速衰老过程。最近的研究表明,衰老细胞和癌细胞一样,会表达某些类型的免疫检查点蛋白以及非经典的免疫耐受 MHC 变异体,从而导致免疫逃逸监视系统。因此,免疫检查点阻断(ICB)可能是一种很有前景的策略,可加强对衰老的免疫监视,从而改善一些与年龄有关的疾病和组织功能障碍。
{"title":"Immune surveillance of senescence: potential application to age-related diseases","authors":"","doi":"10.1016/j.tcb.2024.06.007","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.06.007","url":null,"abstract":"<p>Several lines of evidence suggest that the age-dependent accumulation of senescent cells leads to chronic tissue microinflammation, which in turn contributes to age-related pathologies. In general, senescent cells can be eliminated by the host’s innate and adaptive immune surveillance system, including macrophages, NK cells, and T cells. Impaired immune surveillance leads to the accumulation of senescent cells and accelerates the aging process. Recently, senescent cells, like cancer cells, have been shown to express certain types of immune checkpoint proteins as well as non-classical immune-tolerant MHC variants, leading to immune escape from surveillance systems. Thus, immune checkpoint blockade (ICB) may be a promising strategy to enhance immune surveillance of senescence, leading to the amelioration of some age-related diseases and tissue dysfunction.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":19.0,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141718236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Advisory Board and Contents 咨询委员会和内容
IF 19 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-05 DOI: 10.1016/s0962-8924(24)00125-9
No Abstract
无摘要
{"title":"Advisory Board and Contents","authors":"","doi":"10.1016/s0962-8924(24)00125-9","DOIUrl":"https://doi.org/10.1016/s0962-8924(24)00125-9","url":null,"abstract":"No Abstract","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":19.0,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141546835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Subscription and Copyright Information 订阅和版权信息
IF 19 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-05 DOI: 10.1016/s0962-8924(24)00129-6
No Abstract
无摘要
{"title":"Subscription and Copyright Information","authors":"","doi":"10.1016/s0962-8924(24)00129-6","DOIUrl":"https://doi.org/10.1016/s0962-8924(24)00129-6","url":null,"abstract":"No Abstract","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":19.0,"publicationDate":"2024-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141546837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Filopodia: integrating cellular functions with theoretical models. 丝状体:细胞功能与理论模型的结合。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-04 DOI: 10.1016/j.tcb.2024.05.005
Victoria Thusgaard Ruhoff, Natascha Leijnse, Amin Doostmohammadi, Poul Martin Bendix

Filopodia, widely distributed on cell surfaces, are distinguished by their dynamic extensions, playing pivotal roles in a myriad of biological processes. Their functions span from mechanosensing and guidance to cell-cell communication during cellular organization in the early embryo. Filopodia have significant roles in pathogenic processes, such as cancer invasion and viral dissemination. Molecular mapping of the filopodome has revealed generic components essential for filopodia functions. In parallel, recent insights into biophysical mechanisms governing filopodia dynamics have provided the foundation for broader investigations of filopodia's biological functions. We highlight recent discoveries of engagement of filopodia in various stages of development and pathogenesis and present an overview of intricate molecular and physical features of these cellular structures across a spectrum of cellular activities.

丝状体广泛分布于细胞表面,以其动态延伸而著称,在无数生物过程中发挥着关键作用。它们的功能包括早期胚胎细胞组织过程中的机械传感和引导,以及细胞间的交流。丝状体在癌症侵袭和病毒传播等致病过程中发挥着重要作用。丝状体的分子图谱揭示了丝状体功能所必需的一般成分。与此同时,最近对支配丝状体动力学的生物物理机制的深入了解为更广泛地研究丝状体的生物功能奠定了基础。我们重点介绍了最近发现的丝状体在发育和致病的各个阶段的参与情况,并概述了这些细胞结构在各种细胞活动中错综复杂的分子和物理特征。
{"title":"Filopodia: integrating cellular functions with theoretical models.","authors":"Victoria Thusgaard Ruhoff, Natascha Leijnse, Amin Doostmohammadi, Poul Martin Bendix","doi":"10.1016/j.tcb.2024.05.005","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.05.005","url":null,"abstract":"<p><p>Filopodia, widely distributed on cell surfaces, are distinguished by their dynamic extensions, playing pivotal roles in a myriad of biological processes. Their functions span from mechanosensing and guidance to cell-cell communication during cellular organization in the early embryo. Filopodia have significant roles in pathogenic processes, such as cancer invasion and viral dissemination. Molecular mapping of the filopodome has revealed generic components essential for filopodia functions. In parallel, recent insights into biophysical mechanisms governing filopodia dynamics have provided the foundation for broader investigations of filopodia's biological functions. We highlight recent discoveries of engagement of filopodia in various stages of development and pathogenesis and present an overview of intricate molecular and physical features of these cellular structures across a spectrum of cellular activities.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141538994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Regulated circRNA nuclear export in neuronal differentiation 神经元分化过程中受调控的 circRNA 核输出
IF 19 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-03 DOI: 10.1016/j.tcb.2024.06.005
Da Li, Yingqun Huang

Multiple mechanisms have been reported for how circular RNAs (circRNAs) are exported to the cytoplasm. A recent paper by Cao et al. shows that export of a subset of circRNAs with (A)-rich motifs, including one with a clear function, is regulated during neuronal development via a novel mechanism.

关于环状 RNA(circRNA)如何输出到细胞质,已有多种机制的报道。Cao 等人最近的一篇论文表明,在神经元发育过程中,具有富含 (A) 基序的 circRNAs 子集(包括一种具有明确功能的 circRNAs)的输出是通过一种新的机制进行调控的。
{"title":"Regulated circRNA nuclear export in neuronal differentiation","authors":"Da Li, Yingqun Huang","doi":"10.1016/j.tcb.2024.06.005","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.06.005","url":null,"abstract":"<p>Multiple mechanisms have been reported for how circular RNAs (circRNAs) are exported to the cytoplasm. A recent paper by <span>Cao <em>et al.</em></span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"8px\" viewbox=\"0 0 8 8\" width=\"8px\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg> shows that export of a subset of circRNAs with (A)-rich motifs, including one with a clear function, is regulated during neuronal development via a novel mechanism.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":19.0,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141517066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Deciphering the significance of p53 mutant proteins. 解密 p53 突变蛋白的意义。
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-02 DOI: 10.1016/j.tcb.2024.06.003
Alessio Butera, Ivano Amelio

Mutations in the p53 gene compromise its role as guardian of genomic integrity, yielding predominantly missense p53 mutant proteins. The gain-of-function hypothesis has long suggested that these mutant proteins acquire new oncogenic properties; however, recent studies challenge this notion, indicating that targeting these mutants may not impact the fitness of cancer cells. Mounting evidence indicates that tumorigenesis involves a cooperative interplay between driver mutations and cellular state, influenced by developmental stage, external insults, and tissue damage. Consistently, the behavior and properties of p53 mutants are altered by the context. This article aims to provide a balanced summary of the evolving evidence regarding the contribution of p53 mutants in the biology of cancer while contemplating alternative frameworks to decipher the complexity of p53 mutants within their physiological contexts.

p53 基因的突变损害了其作为基因组完整性守护者的作用,主要产生错义 p53 突变蛋白。长期以来,功能增益假说一直认为这些突变蛋白具有新的致癌特性;然而,最近的研究对这一观点提出了质疑,表明针对这些突变体可能不会影响癌细胞的健康。越来越多的证据表明,肿瘤发生涉及驱动突变和细胞状态之间的合作性相互作用,并受到发育阶段、外部损伤和组织损伤的影响。p53突变体的行为和特性始终受环境影响而改变。本文旨在对有关 p53 突变体在癌症生物学中的作用的不断演变的证据进行平衡的总结,同时考虑采用其他框架来解读 p53 突变体在其生理环境中的复杂性。
{"title":"Deciphering the significance of p53 mutant proteins.","authors":"Alessio Butera, Ivano Amelio","doi":"10.1016/j.tcb.2024.06.003","DOIUrl":"https://doi.org/10.1016/j.tcb.2024.06.003","url":null,"abstract":"<p><p>Mutations in the p53 gene compromise its role as guardian of genomic integrity, yielding predominantly missense p53 mutant proteins. The gain-of-function hypothesis has long suggested that these mutant proteins acquire new oncogenic properties; however, recent studies challenge this notion, indicating that targeting these mutants may not impact the fitness of cancer cells. Mounting evidence indicates that tumorigenesis involves a cooperative interplay between driver mutations and cellular state, influenced by developmental stage, external insults, and tissue damage. Consistently, the behavior and properties of p53 mutants are altered by the context. This article aims to provide a balanced summary of the evolving evidence regarding the contribution of p53 mutants in the biology of cancer while contemplating alternative frameworks to decipher the complexity of p53 mutants within their physiological contexts.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141499653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Glial plasticity in the zebrafish central nervous system. 斑马鱼中枢神经系统的神经胶质可塑性
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-01 Epub Date: 2024-05-16 DOI: 10.1016/j.tcb.2024.04.006
Clara Mutschler, Stephanie B Telerman

Glial cells have a remarkable plasticity. Recent studies using zebrafish as a model highlight conserved cellular behavior in health and disease in the central nervous system (CNS) between zebrafish and humans. These findings inform our understanding of their function and how their dysregulation in pathogenesis can be determinant.

神经胶质细胞具有显著的可塑性。以斑马鱼为模型的最新研究强调了斑马鱼和人类在中枢神经系统(CNS)的健康和疾病中细胞行为的一致性。这些发现有助于我们了解神经胶质细胞的功能,以及它们在发病过程中的失调如何起决定性作用。
{"title":"Glial plasticity in the zebrafish central nervous system.","authors":"Clara Mutschler, Stephanie B Telerman","doi":"10.1016/j.tcb.2024.04.006","DOIUrl":"10.1016/j.tcb.2024.04.006","url":null,"abstract":"<p><p>Glial cells have a remarkable plasticity. Recent studies using zebrafish as a model highlight conserved cellular behavior in health and disease in the central nervous system (CNS) between zebrafish and humans. These findings inform our understanding of their function and how their dysregulation in pathogenesis can be determinant.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140961092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Driving factors of neuronal ferroptosis. 神经元铁变态反应的驱动因素
IF 13 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-07-01 Epub Date: 2024-02-23 DOI: 10.1016/j.tcb.2024.01.010
Julie Jacquemyn, Isha Ralhan, Maria S Ioannou

Ferroptosis is an oxidative form of iron-dependent cell death characterized by the accumulation of lipid peroxides on membranes. Iron and lipids containing polyunsaturated fatty acids are essential for this process. Ferroptosis is central to several neurological diseases and underlies the importance of balanced iron and polyunsaturated fatty acid metabolism in the brain, particularly in neurons. Here, we reflect on the potential links between neuronal physiology and the accumulation of iron and peroxidated lipids, the mechanisms neurons use to protect themselves from ferroptosis, and the relationship between pathogenic protein deposition and ferroptosis in neurodegenerative disease. We propose that the unique physiology of neurons makes them especially vulnerable to ferroptosis.

铁中毒是一种铁依赖性细胞死亡的氧化形式,其特点是膜上脂质过氧化物的积累。铁和含有多不饱和脂肪酸的脂质对这一过程至关重要。铁变态反应是多种神经系统疾病的核心,也是大脑(尤其是神经元)中铁和多不饱和脂肪酸代谢平衡的重要性的基础。在此,我们将探讨神经元生理机能与铁和过氧化脂质积累之间的潜在联系、神经元保护自身免受铁氧化的机制,以及神经退行性疾病中致病蛋白沉积与铁氧化之间的关系。我们提出,神经元独特的生理结构使其特别容易受到铁氧化作用的影响。
{"title":"Driving factors of neuronal ferroptosis.","authors":"Julie Jacquemyn, Isha Ralhan, Maria S Ioannou","doi":"10.1016/j.tcb.2024.01.010","DOIUrl":"10.1016/j.tcb.2024.01.010","url":null,"abstract":"<p><p>Ferroptosis is an oxidative form of iron-dependent cell death characterized by the accumulation of lipid peroxides on membranes. Iron and lipids containing polyunsaturated fatty acids are essential for this process. Ferroptosis is central to several neurological diseases and underlies the importance of balanced iron and polyunsaturated fatty acid metabolism in the brain, particularly in neurons. Here, we reflect on the potential links between neuronal physiology and the accumulation of iron and peroxidated lipids, the mechanisms neurons use to protect themselves from ferroptosis, and the relationship between pathogenic protein deposition and ferroptosis in neurodegenerative disease. We propose that the unique physiology of neurons makes them especially vulnerable to ferroptosis.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":null,"pages":null},"PeriodicalIF":13.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139941261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Trends in Cell Biology
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1