Pub Date : 2025-04-26DOI: 10.1016/j.ceb.2025.102521
Maxx Swoger , Minh Tri Ho Thanh , Alison E. Patteson
Cells must navigate crowded and confining 3D environments during normal function in vivo. Essential to their ability to navigate these environments safely and efficiently is their ability to mediate and endure both self-generated and external forces. The cytoskeleton, composed of F-actin, microtubules, and intermediate filaments, provides the mechanical support necessary for force mediation. The role of F-actin and microtubules in this process has been well studied, whereas vimentin, a cytoplasmic intermediate filament associated with mesenchymal cells, is less studied. However, there is growing evidence that vimentin has functions in both force transmission and protection of the cell from mechanical stress that actin and microtubules cannot fulfill. This review focuses on recent reports highlighting vimentin's role in regulating forces in confining environments.
{"title":"Vimentin – Force regulator in confined environments","authors":"Maxx Swoger , Minh Tri Ho Thanh , Alison E. Patteson","doi":"10.1016/j.ceb.2025.102521","DOIUrl":"10.1016/j.ceb.2025.102521","url":null,"abstract":"<div><div>Cells must navigate crowded and confining 3D environments during normal function <em>in vivo</em>. Essential to their ability to navigate these environments safely and efficiently is their ability to mediate and endure both self-generated and external forces. The cytoskeleton, composed of F-actin, microtubules, and intermediate filaments, provides the mechanical support necessary for force mediation. The role of F-actin and microtubules in this process has been well studied, whereas vimentin, a cytoplasmic intermediate filament associated with mesenchymal cells, is less studied. However, there is growing evidence that vimentin has functions in both force transmission and protection of the cell from mechanical stress that actin and microtubules cannot fulfill. This review focuses on recent reports highlighting vimentin's role in regulating forces in confining environments.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102521"},"PeriodicalIF":6.0,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143877529","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 : 2025-04-22DOI: 10.1016/j.ceb.2025.102519
G. D'Angelo , P.D. Stahl , G. Raposo
Extracellular vesicle (EV) research has expanded beyond traditional boundaries, evolving into an inter-kingdom endeavor. First described over 50 years ago, EVs are now recognized as playing diverse roles in basic cellular functions, such as intercellular communication, transport, and cell migration. Their biogenesis and secretion involve complex molecular processes, with cargos that include proteins, lipids, and genetic material. Despite advances, isolation and purification methods are still developing. EVs are present in all body fluids, with different subtypes fulfilling distinct roles. Nonetheless, in biological ecosystems, vesicle diversity can be seen as a strength where each one complements the other in the dialogue between cells and tissues. The involvement of EVs in homeostasis and disease and their well-recognized potential for diagnosis and therapeutics will continue to boost investigations to reveal their fundamental biology.
{"title":"The cell biology of Extracellular Vesicles: A jigsaw puzzle with a myriad of pieces","authors":"G. D'Angelo , P.D. Stahl , G. Raposo","doi":"10.1016/j.ceb.2025.102519","DOIUrl":"10.1016/j.ceb.2025.102519","url":null,"abstract":"<div><div>Extracellular vesicle (EV) research has expanded beyond traditional boundaries, evolving into an inter-kingdom endeavor. First described over 50 years ago, EVs are now recognized as playing diverse roles in basic cellular functions, such as intercellular communication, transport, and cell migration. Their biogenesis and secretion involve complex molecular processes, with cargos that include proteins, lipids, and genetic material. Despite advances, isolation and purification methods are still developing. EVs are present in all body fluids, with different subtypes fulfilling distinct roles. Nonetheless, in biological ecosystems, vesicle diversity can be seen as a strength where each one complements the other in the dialogue between cells and tissues. The involvement of EVs in homeostasis and disease and their well-recognized potential for diagnosis and therapeutics will continue to boost investigations to reveal their fundamental biology.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102519"},"PeriodicalIF":6.0,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143854838","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 : 2025-04-21DOI: 10.1016/j.ceb.2025.102515
Jan van der Beek, Judith Klumperman
The endo-lysosomal system plays a crucial role in cellular homeostasis by continuously turning over organelles, proteins, and other cargo of intra- or extracellular origin. Moreover, it senses the nutrient status within the cell and can ignite cellular responses by activating or repressing signaling pathways. To enable these roles, lysosomes are fueled by the biosynthetic pathway and receive cargo for degradation by endocytosis and autophagy. Tight regulation and coordination of these distinct trafficking pathways to lysosomes are critical for cellular health. In this review, we explore how these pathways converge at the late stages of the endo-lysosomal system and highlight the role of the HOPS complex as a unifying gatekeeper for trafficking to the lysosome.
{"title":"Trafficking to the lysosome: HOPS paves the way","authors":"Jan van der Beek, Judith Klumperman","doi":"10.1016/j.ceb.2025.102515","DOIUrl":"10.1016/j.ceb.2025.102515","url":null,"abstract":"<div><div>The endo-lysosomal system plays a crucial role in cellular homeostasis by continuously turning over organelles, proteins, and other cargo of intra- or extracellular origin. Moreover, it senses the nutrient status within the cell and can ignite cellular responses by activating or repressing signaling pathways. To enable these roles, lysosomes are fueled by the biosynthetic pathway and receive cargo for degradation by endocytosis and autophagy. Tight regulation and coordination of these distinct trafficking pathways to lysosomes are critical for cellular health. In this review, we explore how these pathways converge at the late stages of the endo-lysosomal system and highlight the role of the HOPS complex as a unifying gatekeeper for trafficking to the lysosome.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102515"},"PeriodicalIF":6.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852271","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 : 2025-04-21DOI: 10.1016/j.ceb.2025.102520
Patrick J. Woida, Rebecca L. Lamason
Eukaryotic cell membranes are protective barriers that precisely control cargo import, trafficking, and export. In defiance of this control, intracellular bacterial pathogens forcefully invade host cells and establish intracellular niches. These pathogens require remarkable membrane remodeling events to support their large size, and a significant amount of work has examined how these pathogens co-opt cytoskeleton dynamics to remodel host membranes. Until recently, less attention was given to where the membranes came from to support remodeling around the pathogens at each stage of infection. In this review, we highlight recent examples of how bacterial pathogens reroute membrane trafficking to provide the membranes needed during invasion, intracellular growth, and eventual dissemination through host tissues. The examples discussed underscore emerging themes and areas for continued investigation rather than provide a survey of the entire field. We hope that highlighting these open questions will inspire researchers across disciplines to recognize the importance of pathogens as tools to understand both mechanisms of bacterial virulence and membrane trafficking.
{"title":"Pathogen-induced rerouting of host membrane trafficking","authors":"Patrick J. Woida, Rebecca L. Lamason","doi":"10.1016/j.ceb.2025.102520","DOIUrl":"10.1016/j.ceb.2025.102520","url":null,"abstract":"<div><div>Eukaryotic cell membranes are protective barriers that precisely control cargo import, trafficking, and export. In defiance of this control, intracellular bacterial pathogens forcefully invade host cells and establish intracellular niches. These pathogens require remarkable membrane remodeling events to support their large size, and a significant amount of work has examined how these pathogens co-opt cytoskeleton dynamics to remodel host membranes. Until recently, less attention was given to where the membranes came from to support remodeling around the pathogens at each stage of infection. In this review, we highlight recent examples of how bacterial pathogens reroute membrane trafficking to provide the membranes needed during invasion, intracellular growth, and eventual dissemination through host tissues. The examples discussed underscore emerging themes and areas for continued investigation rather than provide a survey of the entire field. We hope that highlighting these open questions will inspire researchers across disciplines to recognize the importance of pathogens as tools to understand both mechanisms of bacterial virulence and membrane trafficking.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102520"},"PeriodicalIF":6.0,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852272","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 : 2025-04-19DOI: 10.1016/j.ceb.2025.102516
Brett M. Collins , Peter J. Cullen
The retromer complex was discovered in Saccharomyces cerevisiae as a multiprotein, pentameric assembly essential for recycling of integral membrane cargo proteins through the endosomal network [1,2]. We now understand how retromer is assembled, its membrane architecture, and how it selects proteins for recycling [3–6]. Conserved across eukaryotes, analyses have revealed retromer's role in organism development, and homeostasis and has linked retromer defects with age-related Alzheimer's disease and Parkinson's disease and other neurological disorders [3,5,7]. Indeed, stabilizing retromer function is now actively considered a therapeutic strategy [8]. Here, we reflect on its structural and functional evolution rather than overviewing retromer biology (see, e.g. [5,7]). Specifically, we clarify the organization of the human retromer to provide greater focus for future research, especially within the context of retromer's function in neuroprotection.
{"title":"Separation of powers: A key feature underlying the neuroprotective role of Retromer in age-related neurodegenerative disease?","authors":"Brett M. Collins , Peter J. Cullen","doi":"10.1016/j.ceb.2025.102516","DOIUrl":"10.1016/j.ceb.2025.102516","url":null,"abstract":"<div><div>The retromer complex was discovered in <em>Saccharomyces cerevisiae</em> as a multiprotein, pentameric assembly essential for recycling of integral membrane cargo proteins through the endosomal network [1,2]. We now understand how retromer is assembled, its membrane architecture, and how it selects proteins for recycling [3–6]. Conserved across eukaryotes, analyses have revealed retromer's role in organism development, and homeostasis and has linked retromer defects with age-related Alzheimer's disease and Parkinson's disease and other neurological disorders [3,5,7]. Indeed, stabilizing retromer function is now actively considered a therapeutic strategy [8]. Here, we reflect on its structural and functional evolution rather than overviewing retromer biology (see, <em>e.g.</em> [5,7]). Specifically, we clarify the organization of the human retromer to provide greater focus for future research, especially within the context of retromer's function in neuroprotection.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102516"},"PeriodicalIF":6.0,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143850350","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 : 2025-04-16DOI: 10.1016/j.ceb.2025.102517
Zara L. Ridgway, Xuan Li
Cardiomyocyte signalling pathways are central to maintaining the structural and functional integrity of the heart. Dysregulation of these pathways contributes to the onset and progression of heart diseases, including heart failure, arrhythmias and cardiomyopathies. This review focuses on very recent work on dysfunctional cardiomyocyte signalling and its role in the pathophysiology of heart disease. We discuss key pathways, including immune signalling within cardiomyocytes, signalling associated with microtubule dysfunction, Hippo-yes-associated protein signalling and adenosine monophosphate-activated protein kinase signalling, highlighting how aberrations in their regulation lead to impaired cardiomyocyte functions and pinpointing the potential therapeutic opportunities in these pathways. This review underscores the complexity of cardiomyocyte signalling networks and emphasises the need for further dissecting signalling pathways to prevent cardiomyocyte dysfunction.
{"title":"Dysfunctional cardiomyocyte signalling and heart disease","authors":"Zara L. Ridgway, Xuan Li","doi":"10.1016/j.ceb.2025.102517","DOIUrl":"10.1016/j.ceb.2025.102517","url":null,"abstract":"<div><div>Cardiomyocyte signalling pathways are central to maintaining the structural and functional integrity of the heart. Dysregulation of these pathways contributes to the onset and progression of heart diseases, including heart failure, arrhythmias and cardiomyopathies. This review focuses on very recent work on dysfunctional cardiomyocyte signalling and its role in the pathophysiology of heart disease. We discuss key pathways, including immune signalling within cardiomyocytes, signalling associated with microtubule dysfunction, Hippo-yes-associated protein signalling and adenosine monophosphate-activated protein kinase signalling, highlighting how aberrations in their regulation lead to impaired cardiomyocyte functions and pinpointing the potential therapeutic opportunities in these pathways. This review underscores the complexity of cardiomyocyte signalling networks and emphasises the need for further dissecting signalling pathways to prevent cardiomyocyte dysfunction.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102517"},"PeriodicalIF":6.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143839105","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 : 2025-04-15DOI: 10.1016/j.ceb.2025.102518
Surabhi Sharma , Jyoti Das , Deepa Subramanyam
Intracellular trafficking is known to regulate the outcomes of cellular signalling, with its role in signal generation, reception and interpretation well appreciated. Trafficking within cells can control ligand release, generate and maintain morphogen gradients, regulate ligand uptake within a cell and integrate multiple signals that ultimately result in altered gene expression. This process is especially important over the course of development of multicellular organisms wherein signals within a developing embryo result in the generation of specialized cells.
In this review, we discuss recent developments in our understanding of how intracellular trafficking modulates signalling output and ultimately, cellular identity and highlight recent findings that help us advance our understanding of how the cross talk between trafficking and cell signalling dictates cell fate.
{"title":"Traffic flow and signals: Regulating the movement within cells","authors":"Surabhi Sharma , Jyoti Das , Deepa Subramanyam","doi":"10.1016/j.ceb.2025.102518","DOIUrl":"10.1016/j.ceb.2025.102518","url":null,"abstract":"<div><div>Intracellular trafficking is known to regulate the outcomes of cellular signalling, with its role in signal generation, reception and interpretation well appreciated. Trafficking within cells can control ligand release, generate and maintain morphogen gradients, regulate ligand uptake within a cell and integrate multiple signals that ultimately result in altered gene expression. This process is especially important over the course of development of multicellular organisms wherein signals within a developing embryo result in the generation of specialized cells.</div><div>In this review, we discuss recent developments in our understanding of how intracellular trafficking modulates signalling output and ultimately, cellular identity and highlight recent findings that help us advance our understanding of how the cross talk between trafficking and cell signalling dictates cell fate.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102518"},"PeriodicalIF":6.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143835111","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 : 2025-04-14DOI: 10.1016/j.ceb.2025.102511
Eleni Papafilippou , Lucia Baldauf , Guillaume Charras , Alexandre J. Kabla , Alessandra Bonfanti
Epithelial tissues are continuously exposed to cyclic stretch in vivo. Physiological stretching has been found to regulate soft tissue function at the molecular, cellular, and tissue scales, allowing tissues to preserve their homeostasis and adapt to challenges. In contrast, dysregulated or pathological stretching can induce damage and tissue fragilisation. Many mechanisms have been described for the repair of epithelial tissues across a range of timescales. In this review, we present the timescales of (i) physiological cyclic loading regimes, (ii) strain-regulated remodeling and damage accumulation, and (iii) repair mechanisms in epithelial tissues. We discuss how the response to cyclic loading in biological tissues differs from synthetic materials, in that damage can be partially or fully reversed by repair mechanisms acting on timescales shorter than cyclic loading. We highlight that timescales are critical to understanding the interplay between damage and repair in tissues that experience cyclic loading, opening up new avenues for exploring soft tissue homeostasis.
{"title":"Interplay of damage and repair in the control of epithelial tissue integrity in response to cyclic loading","authors":"Eleni Papafilippou , Lucia Baldauf , Guillaume Charras , Alexandre J. Kabla , Alessandra Bonfanti","doi":"10.1016/j.ceb.2025.102511","DOIUrl":"10.1016/j.ceb.2025.102511","url":null,"abstract":"<div><div>Epithelial tissues are continuously exposed to cyclic stretch <em>in vivo</em>. Physiological stretching has been found to regulate soft tissue function at the molecular, cellular, and tissue scales, allowing tissues to preserve their homeostasis and adapt to challenges. In contrast, dysregulated or pathological stretching can induce damage and tissue fragilisation. Many mechanisms have been described for the repair of epithelial tissues across a range of timescales. In this review, we present the timescales of (i) physiological cyclic loading regimes, (ii) strain-regulated remodeling and damage accumulation, and (iii) repair mechanisms in epithelial tissues. We discuss how the response to cyclic loading in biological tissues differs from synthetic materials, in that damage can be partially or fully reversed by repair mechanisms acting on timescales shorter than cyclic loading. We highlight that timescales are critical to understanding the interplay between damage and repair in tissues that experience cyclic loading, opening up new avenues for exploring soft tissue homeostasis.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102511"},"PeriodicalIF":6.0,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826378","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 : 2025-04-13DOI: 10.1016/j.ceb.2025.102512
Lisa Donker, Susana A. Godinho
Ever since its discovery, acetylation of α-tubulin on lysine 40 (K40) has been associated with the presence of long-lived, stable microtubules. Indeed, later studies revealed that acetylation protects microtubules from mechanical breakage, yet the functional consequences of this modification at the cellular level are only beginning to emerge. Here, we outline novel insights into the mechanisms controlling tubulin acetylation, and its impact on microtubule properties and cellular functions. Finally, we highlight recent advances suggesting that tubulin acetylation can also occur as a dynamic modification in response to a variety of cellular stresses. These observations shed new light on the cell biological functions of tubulin acetylation and give rise to the notion that this modification could be a universal mechanism that allows cells to adapt to changes in their environment or intracellular state.
{"title":"Rethinking tubulin acetylation: From regulation to cellular adaptation","authors":"Lisa Donker, Susana A. Godinho","doi":"10.1016/j.ceb.2025.102512","DOIUrl":"10.1016/j.ceb.2025.102512","url":null,"abstract":"<div><div>Ever since its discovery, acetylation of α-tubulin on lysine 40 (K40) has been associated with the presence of long-lived, stable microtubules. Indeed, later studies revealed that acetylation protects microtubules from mechanical breakage, yet the functional consequences of this modification at the cellular level are only beginning to emerge. Here, we outline novel insights into the mechanisms controlling tubulin acetylation, and its impact on microtubule properties and cellular functions. Finally, we highlight recent advances suggesting that tubulin acetylation can also occur as a dynamic modification in response to a variety of cellular stresses. These observations shed new light on the cell biological functions of tubulin acetylation and give rise to the notion that this modification could be a universal mechanism that allows cells to adapt to changes in their environment or intracellular state.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102512"},"PeriodicalIF":6.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823537","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 : 2025-04-13DOI: 10.1016/j.ceb.2025.102513
Roberta Palmulli, Laura M. Machesky
Macropinocytosis is known as nonselective drinking of the cellular milieu for scavenging of nutrients and uptake of extracellular fluids. It has recently gained attention in cancer research, as targeting the uptake of nutrients or chemotherapeutic particles by tumor cells holds promise for new therapeutic interventions. Macropinocytic cups form from actin-based protrusions that coalesce into cups and collapse into large vesicles containing cargoes and transmembrane receptors, which can then be degraded in lysosomes or recycled back to the plasma membrane. How macropinocytosis is triggered and the various ways that cells utilize cargoes are topics of much interest. Here, we discuss emerging evidence that cargo or membrane receptor uptake in macropinocytosis may in some cases be selective and may substantially alter cell surface receptor trafficking and display.
{"title":"Is macropinocytosis more than just a passive gulp?","authors":"Roberta Palmulli, Laura M. Machesky","doi":"10.1016/j.ceb.2025.102513","DOIUrl":"10.1016/j.ceb.2025.102513","url":null,"abstract":"<div><div>Macropinocytosis is known as nonselective drinking of the cellular milieu for scavenging of nutrients and uptake of extracellular fluids. It has recently gained attention in cancer research, as targeting the uptake of nutrients or chemotherapeutic particles by tumor cells holds promise for new therapeutic interventions. Macropinocytic cups form from actin-based protrusions that coalesce into cups and collapse into large vesicles containing cargoes and transmembrane receptors, which can then be degraded in lysosomes or recycled back to the plasma membrane. How macropinocytosis is triggered and the various ways that cells utilize cargoes are topics of much interest. Here, we discuss emerging evidence that cargo or membrane receptor uptake in macropinocytosis may in some cases be selective and may substantially alter cell surface receptor trafficking and display.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102513"},"PeriodicalIF":6.0,"publicationDate":"2025-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143823538","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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号