{"title":"Lessons in longevity from blood stem cells under protein stress.","authors":"André Catic","doi":"10.1016/j.tcb.2025.06.006","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.06.006","url":null,"abstract":"<p><p>Blood stem cells are among the body's longest-living cells despite being highly vulnerable to proteotoxic damage, which accelerates their aging. To maintain protein homeostasis (proteostasis), hematopoietic stem cells (HSCs) employ mechanisms such as reduced translation rates, high chaperone activity, autophagy, and selective protein degradation. These strategies mitigate protein misfolding, maintain quiescence, and preserve regenerative potential. Disruptions in proteostasis can lead to the elimination of impaired HSCs through differentiation or apoptosis, ensuring the integrity of the stem cell pool. Due to the systemic impact of the blood on aging and its experimental and clinical accessibility, investigating HSC proteostasis provides insights into longevity and potential therapeutic strategies. This review examines emerging mechanistic links between proteostasis and HSC fate, concluding with unresolved questions and challenges of the current research.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":18.1,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ATRX loss induces lineage plasticity and squamous-like phenotype to promote colorectal cancer metastasis.","authors":"Yali Chen, Gaili Ji, Peishan Hu, Rong Xiang","doi":"10.1016/j.tcb.2025.07.003","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.07.003","url":null,"abstract":"<p><p>Colorectal cancer (CRC) metastasis is driven by phenotypic plasticity beyond classic epithelial-mesenchymal transition (EMT), including non-canonical lineages such as squamous-like phenotypes. Their regulatory mechanisms and clinical significance remain unclear. In the current issue of Nature, Cammareri et al. identified ATRX loss as a driver of multilineage plasticity, including squamous-like characteristics, linked to increased metastasis and poor clinical outcomes in CRC.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Science in Mexico: a rising force amid adversity.","authors":"Mayra Furlan-Magaril, Víctor Julián Valdés","doi":"10.1016/j.tcb.2025.07.001","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.07.001","url":null,"abstract":"<p><p>Despite its economic and population status, Mexico's scientific output remains under 1% of global production because of low spending on science. Yet, additional challenges, including over-reliance on expensive imported technology, brain drain, and limited private sector investment, further hinder its progress. Nonetheless, significant opportunities exist, such as fostering local biotechnology, enhancing policy continuity, and leveraging new leadership to boost scientific growth. Although focused on Mexico, these insights hold relevance for the broader region of Latin America, a region that shares vast untapped scientific potential.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144719166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Endosome-ER contact sites in phagophore formation.","authors":"Mengnan Xu, Pingping Wang, Xian-Ping Dong","doi":"10.1016/j.tcb.2025.07.002","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.07.002","url":null,"abstract":"<p><p>Autophagy is a crucial 'self-eating' mechanism used by eukaryotic cells to degrade and recycle cytosolic materials. A recent study by Da Graça et al. reports that the dynamic mobilization of endosome-endoplasmic reticulum (ER) contact sites (EERCS) in response to starvation creates a confined environment that facilitates Ca<sup>2+</sup>-dependent phagophore biogenesis.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144700395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Unlocking Latin America´s scientific potential: challenges and opportunities in a globalized world.","authors":"María Chávez-Canales, Lorena Aguilar-Arnal","doi":"10.1016/j.tcb.2025.06.007","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.06.007","url":null,"abstract":"<p><p>Latin America shows increasing scientific potential, with a dedicated and creative research community, driven by resilience and adaptability. However, limited funding, restricted access to cutting-edge technology, bureaucratic barriers, and constantly changing scientific policies continue to hinder its full integration into the international scientific ecosystem. Latin American scientists also suffer from limitations in their visibility on the global stage, often leading to exclusion. Despite these challenges, many success cases in the region highlight how strategic actions based on planned and sustained investments, international collaborations, and a relevant scientific policy positively impact scientific progress. Through this path, Latin America may not only overcome existing barriers but also position itself as a fundamental player in the scientific stage.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144669089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Stem-like cells at the center of CD4 T cell differentiation.","authors":"Maria A Cardenas, Haydn T Kissick","doi":"10.1016/j.tcb.2025.06.004","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.06.004","url":null,"abstract":"<p><p>CD4 T cells orchestrate immune responses through differentiation into specialized helper subsets. Traditionally, CD4 T cell differentiation is described as a linear process in which naïve CD4 T cells commit to distinct effector lineages upon activation. However, growing evidence challenging this paradigm has provoked considerable debate about CD4 T cell plasticity. This review describes the emerging concept of stem-like CD4 T cells and how they update our understanding of the fundamental mechanisms that regulate CD4 T cell differentiation. We discuss how stem-like CD4 T cells play a crucial role as precursor cells to distinct effector subsets and explore their implications in cancer, infections, and autoimmunity. Finally, we address how stem-like CD4 T cells might resolve long-standing questions about CD4 T cell plasticity, and propose alternative differentiation models that incorporate this population in chronic diseases.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144651235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Communicating science in Latin America: insights, challenges, and future directions.","authors":"Cecilia Rosen","doi":"10.1016/j.tcb.2025.06.003","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.06.003","url":null,"abstract":"<p><p>This article reviews public science communication (SC) in Latin America, highlighting advances and challenges. It emphasizes the need to foster inclusive policies, interdisciplinary approaches, and effective evaluation to enhance public engagement, address social inequalities, and foster informed decision-making. Improving this field would strengthen science-society relationships, benefiting both professional communicators and scientific communities.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gabriel J Pascal, Sadie Kim, Christopher Xie, Dipon Mondal, Renato V Iozzo
{"title":"Proteoglycans are protagonists in autophagy, lymphangiogenesis, and neurodegenerative diseases.","authors":"Gabriel J Pascal, Sadie Kim, Christopher Xie, Dipon Mondal, Renato V Iozzo","doi":"10.1016/j.tcb.2025.06.002","DOIUrl":"10.1016/j.tcb.2025.06.002","url":null,"abstract":"<p><p>Proteoglycans (PGs) are specialized cell-surface and secreted proteins teeming with bioactivity. They have been the subject of fascinating research on autophagy, lymphangiogenesis, and neurodegenerative diseases. PG influence on autophagy extends to several disease domains, and their ability to alter autophagic processes has highlighted their suitability as therapeutic targets. PGs also display new functions by evoking protracted autophagy in lymphatic endothelial cells and inhibiting tumor and physiological lymphangiogenesis. The variable degree of PG sulfation and their ability to regulate growth-factor activities in the central nervous system has opened doors into novel therapeutic avenues including Alzheimer's and Parkinson's diseases. This review systematically integrates these diverse qualities of PGs while highlighting future directions towards clinical application.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12258961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Mitochondrial DNA: how does it leave mitochondria?","authors":"Vladimir Gogvadze, Boris Zhivotovsky","doi":"10.1016/j.tcb.2025.06.005","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.06.005","url":null,"abstract":"<p><p>In recent years, studies have reported the presence of mitochondrial DNA (mtDNA) in the cytosol. However, a certain number of publications on the mechanisms of mtDNA release contain uncertainties. mtDNA is located in the mitochondrial matrix and cannot be released through the same pathways as intermembrane space proteins. This forum article aims to examine the assumptions and elucidate the processes underlying this phenomenon.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144621262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Luke J Fulcher, Caleb Batley, Tomoaki Sobajima, Francis A Barr
{"title":"Time as a danger signal promoting G1 arrest after mitosis.","authors":"Luke J Fulcher, Caleb Batley, Tomoaki Sobajima, Francis A Barr","doi":"10.1016/j.tcb.2025.06.001","DOIUrl":"https://doi.org/10.1016/j.tcb.2025.06.001","url":null,"abstract":"<p><p>Cell cycle checkpoints preventing the replication and inheritance of damaged DNA are crucial for maintaining genome stability and stopping the growth of damaged cells. Canonical checkpoints do this by preventing passage between cell cycle phases until damage has been repaired, or by promoting cell cycle exit. Herein we review checkpoint integration between cell cycle phases, specifically findings showing that extended spindle assembly checkpoint surveillance in mitosis is a danger signal triggering G1 cell cycle arrest. Evidence linking mitotic delays induced by activation of the spindle assembly checkpoint with positive and negative regulators of the G1 DNA damage checkpoint target p53 is discussed, with a focus on time-dependent changes to a p53-binding deubiquitinating complex USP28-53BP1 and the p53 ubiquitin-ligase mouse double minute homologue 2 (MDM2), respectively.</p>","PeriodicalId":56085,"journal":{"name":"Trends in Cell Biology","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144593006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}