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Emerging challenges, mechanisms, and therapeutic opportunities in cell death 细胞死亡的新挑战、机制和治疗机会
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 DOI: 10.1016/j.chembiol.2026.06.015
Scott J. Dixon, Guido Kroemer, Guillaume Lessene, Judy Lieberman, John Silke
{"title":"Emerging challenges, mechanisms, and therapeutic opportunities in cell death","authors":"Scott J. Dixon,&nbsp;Guido Kroemer,&nbsp;Guillaume Lessene,&nbsp;Judy Lieberman,&nbsp;John Silke","doi":"10.1016/j.chembiol.2026.06.015","DOIUrl":"10.1016/j.chembiol.2026.06.015","url":null,"abstract":"<div><div>Regulated cell death pathways play fundamental roles in development, tissue homeostasis, immunity, and disease, and have emerged as promising targets for therapeutic intervention. In this <em>Cell Chemical Biology</em> special issue on cell death mechanisms, this Voices article brings together researchers from across the field to address the following questions: which recent advances in cell death research excite you most, what key challenges remain, and what are the next big questions in the field?</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 889-891"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148461969","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}
引用次数: 0
Transcending cell death – The diverse roles of necroptosis signal adaptors in pathogen infection 超越细胞死亡——坏死坏死信号接头在病原体感染中的不同作用
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 Epub Date: 2026-03-16 DOI: 10.1016/j.chembiol.2026.02.006
Fangmin Huang, Jianwei Li, Francis Ka-Ming Chan
{"title":"Transcending cell death – The diverse roles of necroptosis signal adaptors in pathogen infection","authors":"Fangmin Huang,&nbsp;Jianwei Li,&nbsp;Francis Ka-Ming Chan","doi":"10.1016/j.chembiol.2026.02.006","DOIUrl":"10.1016/j.chembiol.2026.02.006","url":null,"abstract":"<div><div>Necroptosis is a critical host response against pathogenic challenge. As such, many pathogens have developed strategies to fend off host cell necroptosis. This tug-of-war between the host and pathogen has led to the widely held view that necroptosis evolves primarily as a host response to infection. Paradoxically, pathogens that encode caspase inhibitors and therefore render infected cells sensitive to necroptosis also develop strategies that block necroptosis. Hence, cell death alone may not be sufficient to account for the protective role of necroptosis signal adaptors in host defense. We propose an alternative model in which cell death signal adaptors function as sensors of pathogen-encoded activities. In this scenario, pathogen interference with necroptosis may not only affect host cell death but also tune the magnitude and quality of the ensuing immune response. The crosstalk between necroptosis and other inflammatory cell death programs during viral infection will also be discussed.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 905-913"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462117","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}
引用次数: 0
Pyroptosis across species and its potential impact on host defense against zoonotic pathogens 跨物种热亡及其对宿主防御人畜共患病原体的潜在影响。
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 Epub Date: 2026-06-15 DOI: 10.1016/j.chembiol.2026.05.008
Stella Ho, Clare E. Bryant
{"title":"Pyroptosis across species and its potential impact on host defense against zoonotic pathogens","authors":"Stella Ho,&nbsp;Clare E. Bryant","doi":"10.1016/j.chembiol.2026.05.008","DOIUrl":"10.1016/j.chembiol.2026.05.008","url":null,"abstract":"<div><div>Regulated cell death (RCD) plays a central role in host defenses against infection. It is also an important driver of pathology in sepsis. The proteins that regulate RCD in mice and, to a lesser degree, in humans are increasingly well understood. In other species, how RCD, especially pyroptosis, occurs in response to infection is less clear. In this review, we outline what is currently known about genes involved in RCD with a focus on pyroptosis across different species and consider the potential consequences that the genetic diversity might have on the host response to infection.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 1058-1064"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148256727","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}
引用次数: 0
BACH1 meets its match: Heme licenses BACH1 destruction to tune ferroptosis BACH1遇到了它的对手：血红素允许BACH1破坏以调节铁凋亡
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 DOI: 10.1016/j.chembiol.2026.06.013
Dylan Calhoon, Javier Garcia-Bermudez
{"title":"BACH1 meets its match: Heme licenses BACH1 destruction to tune ferroptosis","authors":"Dylan Calhoon,&nbsp;Javier Garcia-Bermudez","doi":"10.1016/j.chembiol.2026.06.013","DOIUrl":"10.1016/j.chembiol.2026.06.013","url":null,"abstract":"<div><div>In a recent issue of <em>Molecular Cell</em>, Ahmed and colleagues<span><span><sup>1</sup></span></span> show that heme enables CRL2-FEM1B to recognize and degrade BACH1, linking metabolite-assisted substrate recruitment to ferroptosis regulation. This mechanism connects heme sensing, ubiquitin-mediated proteolysis, and transcriptional control of ferroptosis-protective genes, revealing a potential vulnerability in lung cancer.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 894-896"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148461556","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}
引用次数: 0
Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation 感染和炎症中ptm -转换串扰对巨噬细胞死亡的动力学控制。
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 Epub Date: 2026-05-18 DOI: 10.1016/j.chembiol.2026.04.011
Sandhini Saha, Rohit Verma, Aleksandra Nita-Lazar
{"title":"Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation","authors":"Sandhini Saha,&nbsp;Rohit Verma,&nbsp;Aleksandra Nita-Lazar","doi":"10.1016/j.chembiol.2026.04.011","DOIUrl":"10.1016/j.chembiol.2026.04.011","url":null,"abstract":"<div><div>Macrophage fate decisions during infection are commonly framed as receptor-proximal transcriptional choices. We propose that the functional outcome results from a “kinetic race,” a dynamic proteostatic competition among protein synthesis, post-translational modifications (PTMs), and degradation. Building on experimental evidence of infection-induced proteostasis, we outline a conceptual “turnover-first” framework. In this model, we hypothesize that the ubiquitin proteasome system (UPS), autophagy, and translational control create a master molecular timer that licenses or restrains pyroptosis, apoptosis, necroptosis, and PANoptosis. We detail how PTMs act as decision codes and present examples of how bacterial pathogens and viruses hijack this network, deploying specialized effectors to move death thresholds by host shutoff, ubiquitin/ISG15 editing, and autophagy evasion. We summarize the emerging chemical biology platforms allowing quantification of these “death competence codes” in real-time, and map drug-addressable nodes offering a systems level strategy to tune macrophage longevity and inflammatory output in sepsis and infectious disease.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 1038-1057"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13192296/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147969199","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}
引用次数: 0
Meet the authors: Stella Ho and Clare Bryant 来认识一下作者：Stella Ho和Clare Bryant
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 DOI: 10.1016/j.chembiol.2026.06.002
Stella Ho, Clare Elizabeth Bryant
{"title":"Meet the authors: Stella Ho and Clare Bryant","authors":"Stella Ho,&nbsp;Clare Elizabeth Bryant","doi":"10.1016/j.chembiol.2026.06.002","DOIUrl":"10.1016/j.chembiol.2026.06.002","url":null,"abstract":"<div><div>In an interview with Samantha Nelson, a scientific editor of <em>Cell Chemical Biology</em>, the authors of the minireview entitled “Pyroptosis across species and its potential impact on host defense against zoonotic pathogens” share their perspectives on their field and life as scientists.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 892-893"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148461554","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}
引用次数: 0
Beyond the veil of cell death 超越细胞死亡的面纱
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 Epub Date: 2026-07-01 DOI: 10.1016/j.chembiol.2026.05.003
Douglas R. Green, Greisly Nunez, Xiaoyu Zhang
{"title":"Beyond the veil of cell death","authors":"Douglas R. Green,&nbsp;Greisly Nunez,&nbsp;Xiaoyu Zhang","doi":"10.1016/j.chembiol.2026.05.003","DOIUrl":"10.1016/j.chembiol.2026.05.003","url":null,"abstract":"<div><div>Studies of regulated cell death have largely focused on the underlying mechanisms and modalities resulting in cell demise, as well as the biological and pathological consequences of cell death. More recently, at least some attention has turned to other questions: how do cells that engage a regulated cell death pathway sometimes survive? And do such “near-death experiences” alter the biology of the surviving cell? Like Alice passing through the looking glass, this 180° change in perspective may represent a paradigm shift in the field. Here, we discuss the concepts, mechanisms, and potential consequences of cell survival despite engaging a regulated cell death pathway.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 897-904"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366366","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}
引用次数: 0
Too much of a good thing: Promotion of tumor progression and metastasis by apoptotic cells 过量是一件好事：凋亡细胞促进肿瘤进展和转移
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 Epub Date: 2026-03-26 DOI: 10.1016/j.chembiol.2026.02.014
Cassidy E. Hagan, Andrew Oberst
{"title":"Too much of a good thing: Promotion of tumor progression and metastasis by apoptotic cells","authors":"Cassidy E. Hagan,&nbsp;Andrew Oberst","doi":"10.1016/j.chembiol.2026.02.014","DOIUrl":"10.1016/j.chembiol.2026.02.014","url":null,"abstract":"<div><div>Nearly all cancer therapies seek to induce the death of tumor cells. In most cases, they do so by triggering the programmed cell death process of apoptosis, often inducing substantial apoptosis in non-tumor tissues as well as within the tumor itself. Apoptotic cells do not simply disappear from the body; they are cleared by professional and non-professional phagocytes, and during this process, apoptotic cells release soluble signaling molecules and induce phenotypic changes in the phagocytes into which they are absorbed. While much attention has been paid to re-engaging and enhancing tumor cell apoptosis during therapy, emerging evidence suggests that signals emanating from apoptotic cells may promote primary tumor growth and metastatic spread. Here, we summarize the immune suppressive and pro-proliferative effects of apoptotic cells, evidence for their impact on primary tumor growth and metastasis, and strategies that may limit the pro-tumor effects of apoptosis.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 952-965"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147507638","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}
引用次数: 0
Redundant or resilient? A systems view of ferroptosis surveillance mechanisms 冗余还是弹性？铁下垂监测机制的系统观点
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 Epub Date: 2026-01-06 DOI: 10.1016/j.chembiol.2025.11.013
Deguang Liang, Xuejun Jiang
{"title":"Redundant or resilient? A systems view of ferroptosis surveillance mechanisms","authors":"Deguang Liang,&nbsp;Xuejun Jiang","doi":"10.1016/j.chembiol.2025.11.013","DOIUrl":"10.1016/j.chembiol.2025.11.013","url":null,"abstract":"<div><div>Ferroptosis is an iron-dependent form of regulated necrosis driven by phospholipid peroxidation. Its suppression relies on a multilayered surveillance system—including neutralizing phospholipid peroxides, terminating the propagation of lipid peroxidation, and limiting the substrates for phospholipid peroxidation—that operates across subcellular compartments and adapts to tissue-specific demands. Rather than functioning redundantly, these defense mechanisms are deployed in a resilient, context-specific manner, shaped by the metabolic profiles, redox states, and regenerative capacities of distinct cell types. Intact ferroptosis surveillance may be especially crucial for post-mitotic cells such as neurons, as its failure can lead to oxidative damage and irreversible degeneration. In contrast, cancer cells actively acquire ferroptosis resistance by upregulating antioxidant networks and reprogramming lipid metabolism, thereby creating a therapeutic vulnerability. Understanding how ferroptosis surveillance is spatially organized and dynamically regulated provides a framework for precision interventions—restoring redox resilience in degenerative disease or selectively inducing ferroptosis in tumors.</div></div>","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 938-951"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145903110","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}
引用次数: 0
Cell death mechanisms and physiological functions 细胞死亡机制及生理功能
IF 9 1区 生物学
Cell Chemical Biology Pub Date : 2026-07-16 DOI: 10.1016/j.chembiol.2026.06.016
The Cell Chemical Biology editorial team
{"title":"Cell death mechanisms and physiological functions","authors":"The Cell Chemical Biology editorial team","doi":"10.1016/j.chembiol.2026.06.016","DOIUrl":"10.1016/j.chembiol.2026.06.016","url":null,"abstract":"","PeriodicalId":265,"journal":{"name":"Cell Chemical Biology","volume":"33 7","pages":"Pages 887-888"},"PeriodicalIF":9.0,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148462059","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}
引用次数: 0
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