Seminars in cell & developmental biology最新文献

英文中文

Gossiping about death: Apoptosis-induced ERK waves as coordinators of multicellular fate decisions

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-24 DOI: 10.1016/j.semcdb.2025.103615

Paolo Armando Gagliardi , Olivier Pertz

Apoptosis is now recognized as a highly dynamic process that involves the release of a large set of signaling molecules that convey information to cells neighboring an apoptotic site. Recent studies in epithelial systems have discovered that apoptotic cells trigger waves of pulses of mitogen-activated protein kinase (MAPK) / extracellular signal-regulated kinase (ERK) pathway activity in their neighbors. At the single-cell level, the ERK pulses emerge from the MAPK pathway's excitable network properties, such as ultrasensitivity and adaptation. At the cell population level, apoptosis-induced ERK waves (AiEWs) emerge from propagation of ERK pulses across cells via a mechanism that involves mechanical inputs and paracrine signaling. AiEWs enable cell populations to dynamically coordinate fate decision signaling during tissue homeostasis and development. This spatio-temporal signaling mechanism can be hijacked by cancer cells to induce drug-tolerant persister states when apoptosis is triggered by cytotoxic or targeted therapies, undermining treatment efficacy. In this review, we summarize our current understanding of AiEWs, including their initiation, propagation, and coordination of fate decision signaling within a population. We discuss how the relatively simple properties of single cells, and their interactions within a collective coordinate these dynamic signaling patterns. We highlight their implication in resistance to cancer therapy and explore potential strategies to target these waves to re-sensitize cancer cells. Finally, we discuss emerging technologies and future directions to expand the study of this biological phenomenon.

{"title":"Gossiping about death: Apoptosis-induced ERK waves as coordinators of multicellular fate decisions","authors":"Paolo Armando Gagliardi , Olivier Pertz","doi":"10.1016/j.semcdb.2025.103615","DOIUrl":"10.1016/j.semcdb.2025.103615","url":null,"abstract":"<div><div>Apoptosis is now recognized as a highly dynamic process that involves the release of a large set of signaling molecules that convey information to cells neighboring an apoptotic site. Recent studies in epithelial systems have discovered that apoptotic cells trigger waves of pulses of mitogen-activated protein kinase (MAPK) / extracellular signal-regulated kinase (ERK) pathway activity in their neighbors. At the single-cell level, the ERK pulses emerge from the MAPK pathway's excitable network properties, such as ultrasensitivity and adaptation. At the cell population level, apoptosis-induced ERK waves (AiEWs) emerge from propagation of ERK pulses across cells via a mechanism that involves mechanical inputs and paracrine signaling. AiEWs enable cell populations to dynamically coordinate fate decision signaling during tissue homeostasis and development. This spatio-temporal signaling mechanism can be hijacked by cancer cells to induce drug-tolerant persister states when apoptosis is triggered by cytotoxic or targeted therapies, undermining treatment efficacy. In this review, we summarize our current understanding of AiEWs, including their initiation, propagation, and coordination of fate decision signaling within a population. We discuss how the relatively simple properties of single cells, and their interactions within a collective coordinate these dynamic signaling patterns. We highlight their implication in resistance to cancer therapy and explore potential strategies to target these waves to re-sensitize cancer cells. Finally, we discuss emerging technologies and future directions to expand the study of this biological phenomenon.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"171 ","pages":"Article 103615"},"PeriodicalIF":6.2,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143868218","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-17 DOI: 10.1016/j.semcdb.2025.103608

Taylor M. Coughlin , Catherine A. Makarewich

The endoplasmic reticulum (ER) is a multifunctional organelle essential for key cellular processes including protein synthesis, calcium homeostasis, and the cellular stress response. It is composed of distinct domains, such as the rough and smooth ER, as well as membrane regions that facilitate direct communication with other organelles, enabling its diverse functions. While many well-characterized ER proteins contribute to these processes, recent studies have revealed a previously underappreciated class of small proteins that play critical regulatory roles. Microproteins, typically under 100 amino acids in length, were historically overlooked due to size-based biases in genome annotation and often misannotated as noncoding RNAs. Advances in ribosome profiling, mass spectrometry, and computational approaches have now enabled the discovery of numerous previously unrecognized microproteins, significantly expanding our understanding of the proteome. While some ER-associated microproteins, such as phospholamban and sarcolipin, were identified decades ago, newly discovered microproteins share similar fundamental characteristics, underscoring the need to refine our understanding of the coding potential of the genome. Molecular studies have demonstrated that ER microproteins play essential roles in calcium regulation, ER stress response, organelle communication, and protein translocation. Moreover, growing evidence suggests that ER microproteins contribute to cellular homeostasis and are implicated in disease processes, including cardiovascular disease and cancer. This review examines the shared and unique functions of ER microproteins, their implications for health and disease, and their potential as therapeutic targets for conditions associated with ER dysfunction.

{"title":"Emerging roles for microproteins as critical regulators of endoplasmic reticulum function and cellular homeostasis","authors":"Taylor M. Coughlin , Catherine A. Makarewich","doi":"10.1016/j.semcdb.2025.103608","DOIUrl":"10.1016/j.semcdb.2025.103608","url":null,"abstract":"<div><div>The endoplasmic reticulum (ER) is a multifunctional organelle essential for key cellular processes including protein synthesis, calcium homeostasis, and the cellular stress response. It is composed of distinct domains, such as the rough and smooth ER, as well as membrane regions that facilitate direct communication with other organelles, enabling its diverse functions. While many well-characterized ER proteins contribute to these processes, recent studies have revealed a previously underappreciated class of small proteins that play critical regulatory roles. Microproteins, typically under 100 amino acids in length, were historically overlooked due to size-based biases in genome annotation and often misannotated as noncoding RNAs. Advances in ribosome profiling, mass spectrometry, and computational approaches have now enabled the discovery of numerous previously unrecognized microproteins, significantly expanding our understanding of the proteome. While some ER-associated microproteins, such as phospholamban and sarcolipin, were identified decades ago, newly discovered microproteins share similar fundamental characteristics, underscoring the need to refine our understanding of the coding potential of the genome. Molecular studies have demonstrated that ER microproteins play essential roles in calcium regulation, ER stress response, organelle communication, and protein translocation. Moreover, growing evidence suggests that ER microproteins contribute to cellular homeostasis and are implicated in disease processes, including cardiovascular disease and cancer. This review examines the shared and unique functions of ER microproteins, their implications for health and disease, and their potential as therapeutic targets for conditions associated with ER dysfunction.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"170 ","pages":"Article 103608"},"PeriodicalIF":6.2,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143838893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Mechanical force-driven cell competition ensures robust morphogen gradient formation

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-13 DOI: 10.1016/j.semcdb.2025.103607

Kana Aoki , Tohru Ishitani

Morphogen gradients provide positional data and maintain tissue patterns by instructing cells to adopt distinct fates. In contrast, morphogen gradient-forming tissues undergo dynamic morphogenetic movements that generate mechanical forces and can disturb morphogen signal transduction. However, the interactions between morphogen gradients and these forces remain largely unknown. In this study, we described how mechanical force-mediated cell competition corrects noisy morphogen gradients to ensure robust tissue patterns. The Wnt/β-catenin morphogen gradient—that patterns the embryonic anterior-posterior axis—generates cadherin-actomyosin interaction-mediated intercellular tension gradients—termed mechano-gradients. Naturally generated unfit cells that produce noisy Wnt/β-catenin gradients induce local deformation of the mechano-gradients. Neighboring fit cells sense this deformation, resulting in the activation of Piezo family mechanosensitive calcium channels and secretion of annexinA1, which specifically kills unfit cells to recover morphogen gradients. Therefore, mechanical force-mediated cell competition between the morphogen-receiver cells supports robust gradient formation. Additionally, we discuss the potential roles of mechanical force-driven cell competition in other contexts, including organogenesis and cancer.

形态发生梯度提供位置数据，并通过指示细胞采用不同的命运来维持组织模式。相反，形成形态发生梯度的组织会发生动态的形态发生运动，产生机械力并干扰形态发生信号转导。然而，形态发生梯度与这些力之间的相互作用在很大程度上仍是未知的。在这项研究中，我们描述了机械力介导的细胞竞争如何纠正嘈杂的形态发生梯度，以确保稳健的组织模式。Wnt/β-catenin形态发生梯度--胚胎前后轴的模式--产生了由粘连蛋白-肌动蛋白相互作用介导的细胞间张力梯度--即机械梯度。自然生成的不适合细胞会产生嘈杂的 Wnt/β-catenin 梯度，导致机械梯度局部变形。邻近的适合细胞会感知到这种变形，从而激活 Piezo 家族机械敏感钙通道并分泌附件素 A1，专门杀死不适合细胞以恢复形态发生梯度。因此，由机械力介导的形态发生器-受体细胞之间的细胞竞争支持了稳健梯度的形成。此外，我们还讨论了机械力驱动的细胞竞争在器官发生和癌症等其他情况下的潜在作用。

{"title":"Mechanical force-driven cell competition ensures robust morphogen gradient formation","authors":"Kana Aoki , Tohru Ishitani","doi":"10.1016/j.semcdb.2025.103607","DOIUrl":"10.1016/j.semcdb.2025.103607","url":null,"abstract":"<div><div>Morphogen gradients provide positional data and maintain tissue patterns by instructing cells to adopt distinct fates. In contrast, morphogen gradient-forming tissues undergo dynamic morphogenetic movements that generate mechanical forces and can disturb morphogen signal transduction. However, the interactions between morphogen gradients and these forces remain largely unknown. In this study, we described how mechanical force-mediated cell competition corrects noisy morphogen gradients to ensure robust tissue patterns. The Wnt/β-catenin morphogen gradient—that patterns the embryonic anterior-posterior axis—generates cadherin-actomyosin interaction-mediated intercellular tension gradients—termed mechano-gradients. Naturally generated unfit cells that produce noisy Wnt/β-catenin gradients induce local deformation of the mechano-gradients. Neighboring fit cells sense this deformation, resulting in the activation of Piezo family mechanosensitive calcium channels and secretion of annexinA1, which specifically kills unfit cells to recover morphogen gradients. Therefore, mechanical force-mediated cell competition between the morphogen-receiver cells supports robust gradient formation. Additionally, we discuss the potential roles of mechanical force-driven cell competition in other contexts, including organogenesis and cancer.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"170 ","pages":""},"PeriodicalIF":6.2,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Why some hearts heal and others don’t: The phylogenetic landscape of cardiac regenerative capacity

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-11 DOI: 10.1016/j.semcdb.2025.103609

Makoto Nakamura , Guo N. Huang

The limited ability of adult humans to replenish lost heart muscle cells after a heart attack has attracted scientists to explore natural heart regeneration capabilities in the animal kingdom. In particular, research has accelerated since the landmark discovery more than twenty years ago that zebrafish can completely regrow myocardial tissue. In this review, we survey heart regeneration studies in diverse model and non-model animals, aiming to gain insights into both the evolutionary trends in cardiac regenerative potential and the variations among closely related species. Differences in cardiomyogenesis, vasculature formation, and the communication between cardiovascular cells and other players have been investigated to understand the cellular basis, although the precise molecular and genetic causes underlying the stark differences in cardiac regenerative potential among certain close cousins remain largely unknown. By studying cardiovascular regeneration and repair in diverse organisms, we may uncover distinct mechanisms, offering new perspectives for advancing regenerative medicine.

{"title":"Why some hearts heal and others don’t: The phylogenetic landscape of cardiac regenerative capacity","authors":"Makoto Nakamura , Guo N. Huang","doi":"10.1016/j.semcdb.2025.103609","DOIUrl":"10.1016/j.semcdb.2025.103609","url":null,"abstract":"<div><div>The limited ability of adult humans to replenish lost heart muscle cells after a heart attack has attracted scientists to explore natural heart regeneration capabilities in the animal kingdom. In particular, research has accelerated since the landmark discovery more than twenty years ago that zebrafish can completely regrow myocardial tissue. In this review, we survey heart regeneration studies in diverse model and non-model animals, aiming to gain insights into both the evolutionary trends in cardiac regenerative potential and the variations among closely related species. Differences in cardiomyogenesis, vasculature formation, and the communication between cardiovascular cells and other players have been investigated to understand the cellular basis, although the precise molecular and genetic causes underlying the stark differences in cardiac regenerative potential among certain close cousins remain largely unknown. By studying cardiovascular regeneration and repair in diverse organisms, we may uncover distinct mechanisms, offering new perspectives for advancing regenerative medicine.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"170 ","pages":"Article 103609"},"PeriodicalIF":6.2,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143815656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Cardiac enhancers: Gateway to the regulatory mechanisms of heart regeneration

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-10 DOI: 10.1016/j.semcdb.2025.103610

Ian J. Begeman, Megan E. Guyer, Junsu Kang

The adult mammalian heart has limited regenerative capacity. Cardiac injury, such as a myocardial infarction (MI), leads to permanent scarring and impaired heart function. In contrast, neonatal mice and zebrafish possess the ability to repair injured hearts. Cardiac regeneration is driven by profound transcriptional changes, which are controlled by gene regulatory elements, such as tissue regeneration enhancer elements (TREEs). Here, we review recent studies on cardiac injury/regeneration enhancers across species. We further explore regulatory mechanisms governing TREE activities and their associated binding regulators. We also discuss the potential of TREE engineering and how these enhancers can be utilized for heart repair. Decoding the regulatory logic of cardiac regeneration enhancers presents a promising avenue for understanding heart regeneration and advancing therapeutic strategies for heart failure.

引用次数: 0

Geometric factors for cell arrangement: How do cells determine their position in vivo?

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-05 DOI: 10.1016/j.semcdb.2025.103604

Sungrim Seirin-Lee , Akatsuki Kimura

The spatial arrangement of cells plays a crucial role in ensuring robust development of organisms, directing cells to their specific fates in the right place and at the right time. In early embryogenesis, the cell arrangement is determined by several factors such as the cell division axis, cell-cell interactions, and surrounding geometric constraints. While many species utilize similar principles to determine the cell arrangement, the precise dynamics of cell arrangement differ among species, even at early stages. In particular, geometric constraints significantly impact cell arrangement. Nematode species exhibit diverse cell arrangement dynamics due to their rigid eggshells, which intensively confine the internal cells. In this paper, we review the mechanisms of cell arrangement with a focus on geometric constraints, drawing from interdisciplinary perspectives. We also review mathematical models developed to enhance our understanding of these mechanisms and discuss future directions for theoretical approaches in exploring geometric effects on cell arrangement in various tissues of various species.

{"title":"Geometric factors for cell arrangement: How do cells determine their position in vivo?","authors":"Sungrim Seirin-Lee , Akatsuki Kimura","doi":"10.1016/j.semcdb.2025.103604","DOIUrl":"10.1016/j.semcdb.2025.103604","url":null,"abstract":"<div><div>The spatial arrangement of cells plays a crucial role in ensuring robust development of organisms, directing cells to their specific fates in the right place and at the right time. In early embryogenesis, the cell arrangement is determined by several factors such as the cell division axis, cell-cell interactions, and surrounding geometric constraints. While many species utilize similar principles to determine the cell arrangement, the precise dynamics of cell arrangement differ among species, even at early stages. In particular, geometric constraints significantly impact cell arrangement. Nematode species exhibit diverse cell arrangement dynamics due to their rigid eggshells, which intensively confine the internal cells. In this paper, we review the mechanisms of cell arrangement with a focus on geometric constraints, drawing from interdisciplinary perspectives. We also review mathematical models developed to enhance our understanding of these mechanisms and discuss future directions for theoretical approaches in exploring geometric effects on cell arrangement in various tissues of various species.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"169 ","pages":"Article 103604"},"PeriodicalIF":6.2,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143777554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cilia and flagella – Current understanding and recent advances in divergent experimental systems

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-04-03 DOI: 10.1016/j.semcdb.2025.103606

Junmin Pan

引用次数: 0

The ever-diversifying landscape of intra-genomic conflict

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-03-26 DOI: 10.1016/j.semcdb.2025.103603

Mia T. Levine, Sarah E. Zanders

引用次数: 0

Cell death in regeneration and cell turnover: Lessons from planarians and Drosophila

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-03-25 DOI: 10.1016/j.semcdb.2025.103605

Teresa Adell, Francesc Cebrià, Josep F. Abril, Sofia J. Araújo, Montserrat Corominas, Marta Morey, Florenci Serras, Cristina González-Estévez

Programmed cell death plays a crucial role during tissue turnover in all animal species, and it is also essential during regeneration, serving as a key signalling mechanism to promote tissue repair and regrowth. In freshwater planarians, remarkable regenerative abilities are supported by neoblasts, a population of adult stem cells, which enable high somatic cell turnover. Cell death in planarians occurs continuously during regeneration and adult homeostasis, underscoring its critical role in tissue remodeling and repair. However, the exact mechanisms regulating cell death in these organisms remain elusive. In contrast, Drosophila melanogaster serves as a powerful model for studying programmed cell death in development, metamorphosis, and adult tissue maintenance, leveraging advanced genetic tools and visualization techniques. In Drosophila, cell death sculpts tissues, eliminates larval structures during metamorphosis, and supports homeostasis in adulthood. Despite limited regenerative capacity compared to planarians, Drosophila provides unique insights into cell death's regulatory mechanisms. Comparative analysis of these two systems highlights both conserved and divergent roles of programmed cell death in tissue renewal and regeneration. This review synthesizes the latest knowledge of programmed cell death in planarians and Drosophila, aiming to illuminate shared principles and system-specific adaptations, with relevance to tissue repair across biological systems.

{"title":"Cell death in regeneration and cell turnover: Lessons from planarians and Drosophila","authors":"Teresa Adell, Francesc Cebrià, Josep F. Abril, Sofia J. Araújo, Montserrat Corominas, Marta Morey, Florenci Serras, Cristina González-Estévez","doi":"10.1016/j.semcdb.2025.103605","DOIUrl":"10.1016/j.semcdb.2025.103605","url":null,"abstract":"<div><div>Programmed cell death plays a crucial role during tissue turnover in all animal species, and it is also essential during regeneration, serving as a key signalling mechanism to promote tissue repair and regrowth. In freshwater planarians, remarkable regenerative abilities are supported by neoblasts, a population of adult stem cells, which enable high somatic cell turnover. Cell death in planarians occurs continuously during regeneration and adult homeostasis, underscoring its critical role in tissue remodeling and repair. However, the exact mechanisms regulating cell death in these organisms remain elusive. In contrast, <em>Drosophila melanogaster</em> serves as a powerful model for studying programmed cell death in development, metamorphosis, and adult tissue maintenance, leveraging advanced genetic tools and visualization techniques. In <em>Drosophila</em>, cell death sculpts tissues, eliminates larval structures during metamorphosis, and supports homeostasis in adulthood. Despite limited regenerative capacity compared to planarians, <em>Drosophila</em> provides unique insights into cell death's regulatory mechanisms. Comparative analysis of these two systems highlights both conserved and divergent roles of programmed cell death in tissue renewal and regeneration. This review synthesizes the latest knowledge of programmed cell death in planarians and <em>Drosophila</em>, aiming to illuminate shared principles and system-specific adaptations, with relevance to tissue repair across biological systems.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"169 ","pages":"Article 103605"},"PeriodicalIF":6.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Death fuels growth: Emerging players bridging apoptosis and cell proliferation in Drosophila and beyond

IF 6.2 2区生物学 Q1 CELL BIOLOGY

Seminars in cell & developmental biology

Pub Date : 2025-03-12 DOI: 10.1016/j.semcdb.2025.103602

Caitlin Hounsell, Yun Fan

Tissue homeostasis relies on a delicate balance between cell death and proliferation. Apoptosis plays a key role not only in removing damaged cells but also in promoting tissue recovery through a process known as apoptosis-induced proliferation (AiP). This review highlights how caspases, c-Jun N-terminal Kinase (JNK), and Reactive Oxygen Species (ROS) bridge cell death and proliferation, as revealed through studies using Drosophila as a model organism. We also compare these findings with advances in other model systems and discuss their broader implications for tissue regeneration and tumorigenesis.

引用次数: 0

下一页尾页

类型

全部化学•材料生命科学医学物理工程技术环境•农林材料科学地球科学法学管理学化学环境科学与生态学计算机科学教育学经济学农林科学人文科学生物学数学物理与天体物理心理学综合性期刊其他工业工程理学历史学农学文学信息工程

数据库

全部 ACS Publications Elsevier ieeexplore Springer The Royal Society of Chemistry Wiley

期刊

Seminars in cell & developmental 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.

﹀