Pub Date : 2025-05-15DOI: 10.1016/j.ceb.2025.102531
Ewan MacDonald , Ludger Johannes , Christian Wunder
The pH balance between extracellular and intracellular space is crucial for a multitude of cellular processes. Real-time observation of pH fluctuations in the range 4–9 in live cells and tissues in a sensitive, non-invasive manner has become feasible with advances in pH quantification by organic dyes, genetically encoded fluorescent proteins, and DNA-based probes. We discuss mechanisms through which pH affects cell cycle, transcription, senescence, neurotransmission, glycolipid-lectin driven endocytosis, tissue remodelling, immune responses, and GPCR signalling. Growth factor-stimulated acidification of the extracellular space notably triggers enzymatic reactions like desialylation at the plasma membrane that control processes involving cell migration and bone resorption. Research into the role of pH in cellular physiology continues to be a fertile ground for discovery that underscores its fundamental importance.
{"title":"Acidification on the plasma membrane","authors":"Ewan MacDonald , Ludger Johannes , Christian Wunder","doi":"10.1016/j.ceb.2025.102531","DOIUrl":"10.1016/j.ceb.2025.102531","url":null,"abstract":"<div><div>The pH balance between extracellular and intracellular space is crucial for a multitude of cellular processes. Real-time observation of pH fluctuations in the range 4–9 in live cells and tissues in a sensitive, non-invasive manner has become feasible with advances in pH quantification by organic dyes, genetically encoded fluorescent proteins, and DNA-based probes. We discuss mechanisms through which pH affects cell cycle, transcription, senescence, neurotransmission, glycolipid-lectin driven endocytosis, tissue remodelling, immune responses, and GPCR signalling. Growth factor-stimulated acidification of the extracellular space notably triggers enzymatic reactions like desialylation at the plasma membrane that control processes involving cell migration and bone resorption. Research into the role of pH in cellular physiology continues to be a fertile ground for discovery that underscores its fundamental importance.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"95 ","pages":"Article 102531"},"PeriodicalIF":6.0,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143947246","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 : 2025-05-09DOI: 10.1016/j.ceb.2025.102528
Marta Casquero-Veiga , Carlos Ceron , Marta Cortes-Canteli
Alzheimer's disease (AD) is characterized by a multifactorial pathophysiology. Beyond its classical hallmarks, growing evidence highlights vascular contributions, including hemostatic dysregulation and a prothrombotic state in AD. This review focuses on recent findings concerning two key blood clot components–fibrin(ogen) and platelets–and their roles in AD pathology, including fibrinogen's abnormal accumulation in the AD brain, its interaction with amyloid-β, together with the associated impacts on clot stability, vascular occlusion, and neuroinflammation; and the potential switch of platelets along the AD continuum from protective to deleterious. This review provides an update on the interplay between vascular dysfunction and AD, underscoring the need for comprehensive integrative research to address AD's complexity and advocating for personalized approaches to tackle this multifaceted disorder.
{"title":"Alzheimer's disease and vascular biology – A focus on the procoagulant state","authors":"Marta Casquero-Veiga , Carlos Ceron , Marta Cortes-Canteli","doi":"10.1016/j.ceb.2025.102528","DOIUrl":"10.1016/j.ceb.2025.102528","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is characterized by a multifactorial pathophysiology. Beyond its classical hallmarks, growing evidence highlights vascular contributions, including hemostatic dysregulation and a prothrombotic state in AD. This review focuses on recent findings concerning two key blood clot components–fibrin(ogen) and platelets–and their roles in AD pathology, including fibrinogen's abnormal accumulation in the AD brain, its interaction with amyloid-β, together with the associated impacts on clot stability, vascular occlusion, and neuroinflammation; and the potential switch of platelets along the AD continuum from protective to deleterious. This review provides an update on the interplay between vascular dysfunction and AD, underscoring the need for comprehensive integrative research to address AD's complexity and advocating for personalized approaches to tackle this multifaceted disorder.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"95 ","pages":"Article 102528"},"PeriodicalIF":6.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143923555","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 : 2025-05-09DOI: 10.1016/j.ceb.2025.102524
Md. Faris H. Ramli , Brian A. Aguado , Jennifer L. Young
During aging, the cardiac extracellular matrix (ECM) undergoes gradual remodeling that reduces the heart's ability to function. Specific ECM changes cause alterations in cellular signaling pathways, eliciting maladaptive responses. Here, we provide insight into the current knowledge of how age-specific ECM changes contribute to altered ligand–receptor interactions, dysregulated mechanotransduction, and the propagation of pro-fibrotic signaling cascades that underpin dysfunction. We also highlight regional and sex differences that new biomolecular and bioengineered technologies have recently uncovered. We call for new biomaterial strategies that mimic spatiotemporal and sex-specific ECM alterations to equip researchers with the tools to unravel complex cellular signaling events. We believe this can be achieved through interdisciplinary cooperation amongst researchers spanning matrix biology, biomaterials, spatial omics, and biomedical engineering.
{"title":"Signals from the extracellular matrix: Region- and sex-specificity in cardiac aging","authors":"Md. Faris H. Ramli , Brian A. Aguado , Jennifer L. Young","doi":"10.1016/j.ceb.2025.102524","DOIUrl":"10.1016/j.ceb.2025.102524","url":null,"abstract":"<div><div>During aging, the cardiac extracellular matrix (ECM) undergoes gradual remodeling that reduces the heart's ability to function. Specific ECM changes cause alterations in cellular signaling pathways, eliciting maladaptive responses. Here, we provide insight into the current knowledge of how age-specific ECM changes contribute to altered ligand–receptor interactions, dysregulated mechanotransduction, and the propagation of pro-fibrotic signaling cascades that underpin dysfunction. We also highlight regional and sex differences that new biomolecular and bioengineered technologies have recently uncovered. We call for new biomaterial strategies that mimic spatiotemporal and sex-specific ECM alterations to equip researchers with the tools to unravel complex cellular signaling events. We believe this can be achieved through interdisciplinary cooperation amongst researchers spanning matrix biology, biomaterials, spatial omics, and biomedical engineering.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"95 ","pages":"Article 102524"},"PeriodicalIF":6.0,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143927459","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 : 2025-05-08DOI: 10.1016/j.ceb.2025.102526
Ana Martin–Vega , Melanie H. Cobb
Numerous stimuli activate the extracellular signal-regulated kinases ERK1/2, which phosphorylate a diverse range of substrates, regulating multiple cellular processes. The broad variety of functions controlled by these enzymes is enabled by complex intracellular organization, which requires precise spatiotemporal regulation. Scaffold proteins and the formation of molecular condensates by liquid–liquid phase separation (LLPS) are key in ERK1/2 signal modulation and output. This review provides an overview of ERK1/2 multifaceted actions, with a focus on the cytoskeleton, mitochondria, and metabolism, as well as ERK1/2 regulation by scaffolds and molecular condensates. We highlight recent findings that shed light on ERK1/2 regulation and discuss the implications for cellular functions, disease mechanisms, and therapeutic development.
{"title":"ERK1/2-MAPK signaling: Metabolic, organellar, and cytoskeletal interactions","authors":"Ana Martin–Vega , Melanie H. Cobb","doi":"10.1016/j.ceb.2025.102526","DOIUrl":"10.1016/j.ceb.2025.102526","url":null,"abstract":"<div><div>Numerous stimuli activate the extracellular signal-regulated kinases ERK1/2, which phosphorylate a diverse range of substrates, regulating multiple cellular processes. The broad variety of functions controlled by these enzymes is enabled by complex intracellular organization, which requires precise spatiotemporal regulation. Scaffold proteins and the formation of molecular condensates by liquid–liquid phase separation (LLPS) are key in ERK1/2 signal modulation and output. This review provides an overview of ERK1/2 multifaceted actions, with a focus on the cytoskeleton, mitochondria, and metabolism, as well as ERK1/2 regulation by scaffolds and molecular condensates. We highlight recent findings that shed light on ERK1/2 regulation and discuss the implications for cellular functions, disease mechanisms, and therapeutic development.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"95 ","pages":"Article 102526"},"PeriodicalIF":6.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143916895","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 : 2025-05-03DOI: 10.1016/j.ceb.2025.102522
Joseph J. Tidei, Patrick W. Oakes, Jordan R. Beach
Cells derive their shape, and in turn much of their behavior, from the organization of the cytoskeleton. While a myriad of proteins contribute to the regulation and organization of this dynamic structure, two of the principal components are actin filaments, which provide the structure, and myosin motors, which generate the majority of the forces. Here we review recent results on the assembly and kinetics of non-muscle myosin 2, and highlight how the cellular environment modulates local myosin behavior and signaling.
{"title":"Myosin 2 – A general contractor for the cytoskeleton","authors":"Joseph J. Tidei, Patrick W. Oakes, Jordan R. Beach","doi":"10.1016/j.ceb.2025.102522","DOIUrl":"10.1016/j.ceb.2025.102522","url":null,"abstract":"<div><div>Cells derive their shape, and in turn much of their behavior, from the organization of the cytoskeleton. While a myriad of proteins contribute to the regulation and organization of this dynamic structure, two of the principal components are actin filaments, which provide the structure, and myosin motors, which generate the majority of the forces. Here we review recent results on the assembly and kinetics of non-muscle myosin 2, and highlight how the cellular environment modulates local myosin behavior and signaling.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102522"},"PeriodicalIF":6.0,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143898981","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 : 2025-04-30DOI: 10.1016/j.ceb.2025.102523
Ding Xiong , Chee San Tong , Min Wu
Calcium (Ca2+) oscillations, marked by periodic fluctuations in cytosolic Ca2+ levels, are a universal feature of both excitable and non-excitable cells, regulating key functions like immune responses, neuronal activity and oocyte activation. Despite significant progress over the past few decades in identifying the molecular toolkits involved in Ca2+ mobilization, fundamental questions remain unresolved: How do Ca2+oscillations arise? In dynamical systems, oscillations arise as closed-loop trajectories in phase space, known as limit cycles. In this framework, [Ca2+] is the variable that oscillates along the limit cycle. Is [Ca2+] also the control parameter that defines the system's stability? Understanding how oscillations arise and how instability is controlled are essential for determining what these oscillations encode. This review revisits classic categorizations of Ca2+ oscillation models, focusing on the minimal mathematical models, their assumptions and gaps linking models with experimental data. We examine historical arguments in light of recent discoveries of plasma membrane lipid oscillations in non-excitable cells. While growing evidence support the pivotal role of lipid signaling in regulating Ca2+ dynamics, they mostly focused on the upstream role of signaling in Ca2+ mobilization, rather than viewing membrane-dependent signal transduction as the core control loop that is responsible for oscillatory Ca2+ dynamics. Here we summarize recent molecular studies of phosphoinositide signaling in modulating Ca2+ dynamics, by considering a broader chemical perspective as essential for understanding Ca2+ oscillations beyond ion fluxes.
{"title":"A molecular systems perspective on calcium oscillations beyond ion fluxes","authors":"Ding Xiong , Chee San Tong , Min Wu","doi":"10.1016/j.ceb.2025.102523","DOIUrl":"10.1016/j.ceb.2025.102523","url":null,"abstract":"<div><div>Calcium (Ca<sup>2+</sup>) oscillations, marked by periodic fluctuations in cytosolic Ca<sup>2+</sup> levels, are a universal feature of both excitable and non-excitable cells, regulating key functions like immune responses, neuronal activity and oocyte activation. Despite significant progress over the past few decades in identifying the molecular toolkits involved in Ca<sup>2+</sup> mobilization, fundamental questions remain unresolved: How do Ca<sup>2+</sup>oscillations arise? In dynamical systems, oscillations arise as closed-loop trajectories in phase space, known as limit cycles. In this framework, [Ca<sup>2+</sup>] is the variable that oscillates along the limit cycle. Is [Ca<sup>2+</sup>] also the control parameter that defines the system's stability? Understanding how oscillations arise and how instability is controlled are essential for determining what these oscillations encode. This review revisits classic categorizations of Ca<sup>2+</sup> oscillation models, focusing on the minimal mathematical models, their assumptions and gaps linking models with experimental data. We examine historical arguments in light of recent discoveries of plasma membrane lipid oscillations in non-excitable cells. While growing evidence support the pivotal role of lipid signaling in regulating Ca<sup>2+</sup> dynamics, they mostly focused on the upstream role of signaling in Ca<sup>2+</sup> mobilization, rather than viewing membrane-dependent signal transduction as the core control loop that is responsible for oscillatory Ca<sup>2+</sup> dynamics. Here we summarize recent molecular studies of phosphoinositide signaling in modulating Ca<sup>2+</sup> dynamics, by considering a broader chemical perspective as essential for understanding Ca<sup>2+</sup> oscillations beyond ion fluxes.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102523"},"PeriodicalIF":6.0,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143891400","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}
Septins are cytoskeletal guanosine triphosphate (GTP)-binding proteins that were discovered in budding yeast and are conserved from algae and protists to mammals. Septins assemble into heteromeric complexes, which can polymerize into filaments and higher-order filament architectures, and perform functions in a wide range of biological processes, including cell division and motility and tissue morphogenesis. Although septin dysfunction in animals is linked to infertility, defective organogenesis, neurodegenerative diseases, and cancer, the molecular mechanisms underlying septin function are not clear. Studies of septins in vivo in whole animals provide a powerful approach for gaining insights into the role of septins in animal pathophysiology and unraveling the molecular and cell biological basis of septin function.
{"title":"Septins in animal tissue architecture: more than just peanuts","authors":"Jyotirmayee Debadarshini, Loïc LeGoff, Manos Mavrakis","doi":"10.1016/j.ceb.2025.102525","DOIUrl":"10.1016/j.ceb.2025.102525","url":null,"abstract":"<div><div>Septins are cytoskeletal guanosine triphosphate (GTP)-binding proteins that were discovered in budding yeast and are conserved from algae and protists to mammals. Septins assemble into heteromeric complexes, which can polymerize into filaments and higher-order filament architectures, and perform functions in a wide range of biological processes, including cell division and motility and tissue morphogenesis. Although septin dysfunction in animals is linked to infertility, defective organogenesis, neurodegenerative diseases, and cancer, the molecular mechanisms underlying septin function are not clear. Studies of septins <em>in vivo</em> in whole animals provide a powerful approach for gaining insights into the role of septins in animal pathophysiology and unraveling the molecular and cell biological basis of septin function.</div></div>","PeriodicalId":50608,"journal":{"name":"Current Opinion in Cell Biology","volume":"94 ","pages":"Article 102525"},"PeriodicalIF":6.0,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143885981","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 : 2025-04-26DOI: 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}
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