Pub Date : 2025-06-01Epub Date: 2025-04-11DOI: 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":"2025-06-01","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}
Pub Date : 2025-06-01Epub Date: 2025-04-13DOI: 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.
{"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":"2025-06-01","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}
Pub Date : 2025-06-01Epub Date: 2025-04-17DOI: 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":"2025-06-01","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}
Pub Date : 2025-06-01Epub Date: 2025-04-10DOI: 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.
{"title":"Cardiac enhancers: Gateway to the regulatory mechanisms of heart regeneration","authors":"Ian J. Begeman, Megan E. Guyer, Junsu Kang","doi":"10.1016/j.semcdb.2025.103610","DOIUrl":"10.1016/j.semcdb.2025.103610","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"170 ","pages":"Article 103610"},"PeriodicalIF":6.2,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143815655","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}
Pub Date : 2025-05-01Epub Date: 2025-03-12DOI: 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.
组织稳态依赖于细胞死亡和增殖之间的微妙平衡。细胞凋亡不仅在清除受损细胞中起着关键作用，而且还通过称为凋亡诱导增殖（AiP）的过程促进组织恢复。本文综述了半胱天冬酶、c-Jun n -末端激酶（JNK）和活性氧（ROS）如何架起细胞死亡和增殖的桥梁，这是通过果蝇作为模式生物的研究发现的。我们还将这些发现与其他模型系统的进展进行了比较，并讨论了它们对组织再生和肿瘤发生的更广泛意义。
{"title":"Death fuels growth: Emerging players bridging apoptosis and cell proliferation in Drosophila and beyond","authors":"Caitlin Hounsell, Yun Fan","doi":"10.1016/j.semcdb.2025.103602","DOIUrl":"10.1016/j.semcdb.2025.103602","url":null,"abstract":"<div><div>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 <em>Drosophila</em> 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.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"169 ","pages":"Article 103602"},"PeriodicalIF":6.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143609166","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}
Pub Date : 2025-05-01Epub Date: 2025-04-03DOI: 10.1016/j.semcdb.2025.103606
Junmin Pan
{"title":"Cilia and flagella – Current understanding and recent advances in divergent experimental systems","authors":"Junmin Pan","doi":"10.1016/j.semcdb.2025.103606","DOIUrl":"10.1016/j.semcdb.2025.103606","url":null,"abstract":"","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"169 ","pages":"Article 103606"},"PeriodicalIF":6.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143759579","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}
Pub Date : 2025-05-01Epub Date: 2025-04-05DOI: 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":"2025-05-01","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}
Pub Date : 2025-05-01Epub Date: 2025-03-25DOI: 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":"2025-05-01","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}
Pub Date : 2025-05-01Epub Date: 2025-03-26DOI: 10.1016/j.semcdb.2025.103603
Mia T. Levine, Sarah E. Zanders
{"title":"The ever-diversifying landscape of intra-genomic conflict","authors":"Mia T. Levine, Sarah E. Zanders","doi":"10.1016/j.semcdb.2025.103603","DOIUrl":"10.1016/j.semcdb.2025.103603","url":null,"abstract":"","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"169 ","pages":"Article 103603"},"PeriodicalIF":6.2,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143697799","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}
Apoptosis is an essential cellular process corresponding to a programmed cell suicide. It has long been considered as a cell-autonomous process, supposed to have no particular impact on the surrounding tissue. However, it has become clear in the last 15 years that epithelial apoptotic cells interact mechanically and biochemically with their environment. Here, we explore recent literature on apoptotic mechanics from an individual dying cell to the back-and-forth interplay with the neighboring epithelial tissue. Finally, we discuss how caspases, key regulators of apoptosis, appear to have a dual function as a cytoskeleton regulator favoring either cytoskeleton degradation or dynamics independently of their apoptotic or non-apoptotic role.
{"title":"Epithelial apoptosis: A back-and-forth mechanical interplay between the dying cell and its surroundings","authors":"Stéphanie Arnould , Corinne Benassayag , Tatiana Merle , Bruno Monier , Marianne Montemurro , Magali Suzanne","doi":"10.1016/j.semcdb.2025.02.001","DOIUrl":"10.1016/j.semcdb.2025.02.001","url":null,"abstract":"<div><div>Apoptosis is an essential cellular process corresponding to a programmed cell suicide. It has long been considered as a cell-autonomous process, supposed to have no particular impact on the surrounding tissue. However, it has become clear in the last 15 years that epithelial apoptotic cells interact mechanically and biochemically with their environment. Here, we explore recent literature on apoptotic mechanics from an individual dying cell to the back-and-forth interplay with the neighboring epithelial tissue. Finally, we discuss how caspases, key regulators of apoptosis, appear to have a dual function as a cytoskeleton regulator favoring either cytoskeleton degradation or dynamics independently of their apoptotic or non-apoptotic role.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"168 ","pages":"Pages 1-12"},"PeriodicalIF":6.2,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143464971","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}
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