Cell Death Discovery最新文献

{"title":"Interplay between ALK2^R206H mutant receptor and autophagy signaling regulates receptor stability and its chondrogenic functions.","authors":"Laura Coculo, Marius Wits, Irene Mariani, Giulia Fianco, Serena Cappato, Renata Bocciardi, Nicoletta Pedemonte, Elisabetta Volpe, Serena Ciolfi, Rosario Luigi Sessa, Serena Rinaldo, Francesca Cutruzzolà, Daniela Trisciuoglio, Marie-Josè Goumans, Gonzalo Sanchez-Duffhues, Venturina Stagni","doi":"10.1038/s41420-025-02393-0","DOIUrl":"10.1038/s41420-025-02393-0","url":null,"abstract":"<p><p>Heterozygous mutations in the Bone morphogenetic protein (BMP) type I receptor ACVR1, encoding activin-like kinase 2 (ALK2), underlie all cases of the rare genetic musculoskeletal disorder Fibrodysplasia Ossificans Progressiva (FOP). The most commonly found mutant ALK2 p.R206H receptor variant exhibits loss of auto inhibition of BMP signaling and can be activated by Activins, while wild-type receptors remain unresponsive. Consequently, the downstream chondrogenic signaling is enhanced, thus driving heterotopic ossification within soft connective tissues. Despite several investigational treatments being evaluated in clinical trials, no cure for FOP exists today. The cellular and molecular mechanisms underlying disease progression are still being deciphered. In this study, we show a close interplay between the mutant ALK2^R206H receptor signaling and dysregulation of the autophagic flux triggered by hypoxia. Mechanistically, reduced autophagic flux correlates with increased stability of ALK2^R206H, resulting in sustained signaling. Of note, we demonstrated that Rapamycin, under clinical investigation as a treatment for FOP, inhibits chondrogenic differentiation in an autophagy-dependent manner. Consistently, other pharmacological autophagy inducers, like Spermidine, can reduce ALK2^R206H driven chondrogenic differentiation in vitro. These results were verified in FOP patient-derived cells. In conclusion, this study shows that aberrant autophagic flux mediates sustained ALK2^R206H signaling, introducing a novel druggable target in FOP by reactivating autophagy.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"117"},"PeriodicalIF":6.1,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11929866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691319","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}

{"title":"Natural products targeting regulated cell deaths for adriamycin-induced cardiotoxicity.","authors":"Zheng Wang, Yanli Zhu, Yu Yao, Wenyu Zhang, Bo Wang, Jing Wang, Yang Yang, Liwen Liu","doi":"10.1038/s41420-025-02389-w","DOIUrl":"10.1038/s41420-025-02389-w","url":null,"abstract":"<p><p>Adriamycin (ADR), as an anti-cancer drug in routine clinical application, is utilized to treat various cancers such as ovarian cancer, hematological malignant tumor, and endometrial carcinoma. However, its serious dose-dependent cardiotoxicity extremely limits its clinical application. Currently, there remains a dearth of therapeutic agents to mitigate ADR-induced cardiotoxicity. Extensive research has demonstrated that ADR can simultaneously trigger various regulated cell death (RCD) pathways, such as apoptosis, autophagy, ferroptosis, necroptosis, and pyroptosis. Therefore, drugs targeting these RCD pathways may represent effective strategies for treating ADR-induced cardiotoxicity. Natural products, with their wide availability, low cost, and diverse pharmacological activities, have increasingly gained attention. Various natural products, including polyphenols, flavonoids, terpenoids, and alkaloids, can target the RCD pathways involved in ADR-induced cardiotoxicity. Furthermore, these natural products have exhibited excellent properties in preclinical studies or in vitro experiments. This review summarizes the mechanisms of RCD in ADR-induced cardiotoxicity and systematically reviews the natural products targeting these RCD pathways. Finally, we propose future research directions of natural products in this field.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"112"},"PeriodicalIF":6.1,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676645","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}

{"title":"Diazinon induces testicular dysfunction and testicular cell damage through increased reactive oxygen species production in mouse.","authors":"Ran Lee, Won-Young Lee, Dong-Wook Kim, Hyun-Jung Park","doi":"10.1038/s41420-025-02399-8","DOIUrl":"10.1038/s41420-025-02399-8","url":null,"abstract":"<p><p>Diazinon (DZN) is an organophosphorus compound used as a pesticide and is an environmentally hazardous substance to which the human body is commonly exposed. In this study, we evaluated the toxicity of DZN to the male reproductive in mice. For in vivo experiments, mice were intraperitoneally injected with 30 mg/kg DZN for 35 days. Microscopic analysis revealed that the diameter of the spermatogonia in the testes decreased, and the number of differentiating germ cells decreased. Sperm motility in mice injected with DZN was reduced, and slow motility was observed. The rate of neck deformation in the sperm increased in DZN-treated mice. The number of germ and Sertoli cells decreased, and the levels of serum testosterone and steroidogenesis markers also decreased in DZN-treated mice. In addition, DZN-induced oxidative stress in the testes. For in vitro experiments, DZN was toxic to GC-1 spermatogonia and TM4 and TM3 cells derived from mouse testes. DZN generated reactive oxygen species (ROS) and induced mitochondrial dysfunction, suggesting a molecular mechanism underlying ROS-induced cell death. DZN upregulated BAD, cleaved-caspase 3, and phospho-p53 at the cellular level. We also found that this toxicity could be mitigated by N-acetyl-l-cysteine, an ROS inhibitor.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"113"},"PeriodicalIF":6.1,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676582","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}

{"title":"Cysteine-rich intestinal protein family: structural overview, functional diversity, and roles in human disease.","authors":"Xilin Ye, Qianben Song, Lumiao Zhang, Mengjia Jing, Yu Fu, Wei Yan","doi":"10.1038/s41420-025-02395-y","DOIUrl":"10.1038/s41420-025-02395-y","url":null,"abstract":"<p><p>The cysteine-rich intestinal protein (CRIP) family, including CRIP1, CRIP2, and CRIP3, is a subfamily of the highly conserved Lin-1, Isl1, Mec3/double zinc finger protein family that exhibits diverse biological functions. The CRIP family is known to play an important role in cellular epithelial-mesenchymal transition, cell death, and tumor progression and participate in multiple signaling pathways. This article summarizes the roles and potential molecular mechanisms of the CRIP family in diseases, which will help to explore new research directions for this family and provide useful information for clinical applications such as disease diagnosis and treatment.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"114"},"PeriodicalIF":6.1,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676580","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}

{"title":"FDX1 overexpression inhibits the growth and metastasis of clear cell renal cell carcinoma by upregulating FMR1 expression.","authors":"Wuping Yang, Cunjin Wu, Chaochao Jiang, Taile Jing, Minghao Lu, Dan Xia, Ding Peng","doi":"10.1038/s41420-025-02380-5","DOIUrl":"10.1038/s41420-025-02380-5","url":null,"abstract":"<p><p>Kidney cancer has caused more than 150,000 deaths in 185 countries around the world and is a serious threat to human life. Clear cell renal cell carcinoma (ccRCC) is the most common type of kidney cancer. FDX1, a crucial gene for regulating copper death, plays an important role in tumors. However, its specific role in ccRCC remains unclear. In this study, by analysing data from the TCGA-KIRC and GEO databases and validation in clinical samples from our center, the expression characteristics of FDX1 and its relationship with tumor clinicopathological features and patient prognosis were clarified; the effects of FDX1 overexpression on ccRCC cell proliferation, apoptosis, migration, and invasion were determined via cell phenotype experiments and mouse orthotopic renal tumor growth models; and the downstream regulatory mechanism of FDX1 was determined via TMT proteomic sequencing, Co-IP assays, and RNA-sequencing detection. Our results confirmed that FDX1 was significantly underexpressed in ccRCC and that reduced FDX1 expression was associated with adverse clinicopathologic features and poor prognosis. FDX1 overexpression markedly inhibited the proliferation, migration, and invasion of ccRCC cells and promoted cell apoptosis in vitro. Mechanistically, FDX1 bound to the FMR1 protein and upregulated its expression, subsequently restraining Bcl-2 and N-cadherin expression and enhancing ALCAM, Cleaved Caspase-3, and E-cadherin expression. In mouse models, FDX1 overexpression significantly suppressed the growth and metastasis of renal tumors, but this inhibitory effect was markedly reversed after FMR1 expression was knocked down. Thus, our results confirmed that FDX1 expression is significantly reduced in ccRCC and serves as a prognostic marker for ccRCC patients and that its overexpression suppresses the growth and metastasis ability of ccRCC by promoting the expression of FRM1.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"115"},"PeriodicalIF":6.1,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11928736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676600","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}

{"title":"New approaches to targeted drug therapy of intracranial tumors.","authors":"Ozal Beylerli, Ilgiz Gareev, Elmar Musaev, Sergey Roumiantsev, Vladimir Chekhonin, Aamir Ahmad, Yuan Chao, Guang Yang","doi":"10.1038/s41420-025-02358-3","DOIUrl":"10.1038/s41420-025-02358-3","url":null,"abstract":"<p><p>Intracranial tumors encompass a heterogeneous group of neoplasms, including gliomas, meningiomas, pituitary adenomas, schwannomas, craniopharyngiomas, ependymomas, medulloblastomas, and primary central nervous system lymphomas. These tumors present significant challenges due to their diverse molecular characteristics, critical locations, and the unique obstacles posed by the blood-brain barrier (BBB) and blood-tumor barrier (BTB), which limit the efficacy of systemic therapies. Recent advances in molecular biology and genomics have enabled the identification of specific molecular pathways and targets, paving the way for innovative precision therapies. This review examines the current state of targeted therapies for intracranial tumors, including receptor tyrosine kinase (RTK) inhibitors, PI3K/AKT/mTOR inhibitors, RAF/MEK/ERK pathway inhibitors, IDH mutation inhibitors, immune checkpoint inhibitors, and CAR-T cell therapies. Emphasis is placed on the role of the BBB and BTB in modulating drug delivery and therapeutic outcomes. Strategies to overcome these barriers, such as focused ultrasound, nanoparticle-based delivery systems, and convection-enhanced delivery, are also explored. Furthermore, the manuscript reviews clinical trial data, highlighting successes and limitations across different tumor types. It delves into emerging therapeutic approaches, including combination of regimens and personalized treatments based on molecular profiling. By synthesizing the latest research, this article aims to provide a comprehensive understanding of the advancements and ongoing challenges in the targeted treatment of intracranial tumors. The findings underscore the necessity for innovative delivery systems and more extensive clinical trials to optimize therapeutic strategies. This review aspires to inform future research and clinical practices, aiming to improve patient outcomes and quality of life in the management of these complex and life-threatening conditions.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"111"},"PeriodicalIF":6.1,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668936","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}

{"title":"MAGL targeted PROTAC degrader simultaneously enhances P53 for synergistic treatment of glioblastoma stem cell.","authors":"Zheng Yuan, Meixia Guo, Yue Zhang, Yilin Deng, Biao Sun, Yaning Hou, Xin Wang, Xiong Jin, Yang Liu, Bingyang Shi, Jinlong Yin","doi":"10.1038/s41420-025-02392-1","DOIUrl":"10.1038/s41420-025-02392-1","url":null,"abstract":"<p><p>Glioblastoma (GBM) stands as the most fatal brain tumor due to limited therapeutic options and high rates of drug resistance. Current surgical and pharmacological interventions usually fail to eradicate the aggressive GBM stem cells (GSCs), which leads to the deadly GBM occurrence. Although proteolysis-targeting chimeras (PROTACs) are prosperous in drug development for tumors, their application in GBM, particularly for GSC-sensitive drug candidates remains in its nascent stages. In this regard, we designed a monoacylglycerol lipase (MAGL) targeting PROTAC, where MAGL was identified as a novel target for GSCs in our previous study. The MAGL inhibitor JZL184 was redesigned by leveraging computational chemistry analysis, and an active unit was engaged for conjugation. E3 ligand for MAGL targeted warhead conjugation was screened with bioinformatics analyses, which revealed heightened activity of the E3 ligase MDM2 in GBM, a classic negative regulator of the tumor suppressor P53, which correlates with patient prognosis. Then the PROTAC was conjugated with JZL184 analog and the MDM2 inhibitor Nutlin-3 analog. Experimental results validated that the designed JN-PROTAC effectively induced MAGL targeted degradation and concomitantly enhanced P53 activation via MDM2 inhibition and is capable of inhibiting the progression of patient-derived GSCs in vivo. This work presents a proof-of-concept PROTAC design tailored for GSCs, potentially addressing the occurrence challenges for GBM.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"109"},"PeriodicalIF":6.1,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668934","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}

{"title":"Targeting Txnip-mediated metabolic reprogramming has therapeutic potential for osteoarthritis.","authors":"Xiankun Cao, Xiao Yang, Pu Zhang, Jianguang Xu, Jie Zhao, Erzhu Yang","doi":"10.1038/s41420-025-02394-z","DOIUrl":"10.1038/s41420-025-02394-z","url":null,"abstract":"<p><p>Osteoarthritis (OA) inflammatory microenvironment triggered glucose metabolism and mitochondrial dysfunction in chondrocytes, leading to a shift of metabolic tendency between oxidative phosphorylation and anaerobic glycolysis. Thioredoxin-interacting protein (Txnip) increased production of reactive oxygen species (ROS), which exacerbates oxidative stress, inflammation and further accelerates cartilage degeneration and extracellular matrix (ECM) degradation. Txnip expression is also positively correlated with several critical pathological glucose and lipid metabolism processes beyond inflammation and endoplasmic reticulum stress (ERS). While the role of Txnip-mediated chondrocyte metabolic reprogramming in OA has not been explored. This study focuses on the unexplored role of Txnip-mediated chondrocyte metabolic reprogramming in chondrogenesis and ECM deposition. The study reveals that upregulated glycolysis after Txnip knockdown significantly contributes to mouse chondrogenesis and ECM deposition. Moreover, verapamil, a clinically used drug that targets Txnip, shows potential for treating mouse OA. These findings suggest that targeting Txnip-mediated metabolic reprogramming could offer a novel therapeutic strategy for OA treatment.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"110"},"PeriodicalIF":6.1,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11926230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668984","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}

{"title":"Lipid metabolism: the potential therapeutic targets in glioblastoma.","authors":"Lu Lu, Yan Zhang, Yuzhong Yang, Meihua Jin, Aiyu Ma, Xu Wang, Qiuyu Zhao, Xuemei Zhang, Jinhua Zheng, Xiang Zheng","doi":"10.1038/s41420-025-02390-3","DOIUrl":"10.1038/s41420-025-02390-3","url":null,"abstract":"<p><p>Glioblastoma is a highly malignant tumor of the central nervous system with a high mortality rate. The mechanisms driving glioblastoma onset and progression are complex, posing substantial challenges for developing precise therapeutic interventions to improve patient survival. Over a century ago, the discovery of the Warburg effect underscored the importance of abnormal glycolysis in tumors, marking a pivotal moment in cancer research. Subsequent studies have identified mitochondrial energy conversion as a fundamental driver of tumor growth. Recently, lipid metabolism has emerged as a critical factor in cancer cell survival, providing an alternative energy source. Research has shown that lipid metabolism is reprogrammed in glioblastoma, playing a vital role in shaping the biological behavior of tumor cells. In this review, we aim to elucidate the impact of lipid metabolism on glioblastoma tumorigenesis and explore potential therapeutic targets. Additionally, we provide insights into the regulatory mechanisms that govern lipid metabolism, emphasizing the critical roles of key genes and regulators involved in this essential metabolic process.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"107"},"PeriodicalIF":6.1,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647333","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}

{"title":"Role of TRIM24 in the regulation of proteasome-autophagy crosstalk in bortezomib-resistant mantle cell lymphoma.","authors":"Corentin Bouvier, Maria Gonzalez-Santamarta, Núria Profitós-Pelejà, Marc Armengol, Grégoire Quinet, Quentin Alasseur, Laurie Ceccato, Wendy Xolalpa, Raimundo Freire, Julie Guillermet-Guibert, Karine Reybier, Anne-Marie Caminade, Hans C Beck, Ana Sofia Carvalho, Rune Matthiesen, Jean Christophe Rain, James D Sutherland, Rosa Barrio, Gaël Roué, Manuel S Rodriguez","doi":"10.1038/s41420-025-02355-6","DOIUrl":"10.1038/s41420-025-02355-6","url":null,"abstract":"<p><p>Resistance to bortezomib (BTZ) represents a major bottleneck to continue using this proteasome inhibitor in the treatment of mantle cell lymphoma (MCL). In this study, we investigated the mechanisms by which TRIM24 (tripartite motif-containing 24), a ubiquitin ligase enriched in the ubiquitome of BTZ-resistant MCL cells, modulates proteasome-autophagy crosstalk. The localization and stability of TRIM24 were differentially influenced by the inhibition of proteasome or autophagy in MCL cells with acquired BTZ resistance (ZBR). Moreover, genetic deletion of the TRIM24 gene in ZBR (ZBR^{TRIM24 KO}) effectively impaired cell proliferation without impacting the degradation of the proteasome by proteaphagy that is typically observed in BTZ-resistant cells. Notably, pre-treatment of ZBR cells with a proteolysis-targeting chimera (PROTAC) targeting TRIM24 (dTRIM24) successfully restored BTZ susceptibility, underscoring the critical role of TRIM24 in mediating resistance to proteasome inhibition. Interestingly, the combined apoptogenic activity of dTRIM24 and BTZ was preserved in a second BTZ-resistant clone (JBR) that lacks functional p53, indicating that this tumor suppressor is not required for the observed effect. Furthermore, we demonstrated that reducing TRIM24 protein levels in BTZ-resistant cells via dTRIM24 treatment restored proteasome activity, facilitating efficient apoptosis induction in cells exposed to the dTRIM24/BTZ combination. Mechanistically, dTRIM24 treatment promoted the formation of K48-linked ubiquitin chains and their association with proteasome subunits, specifically in BTZ-resistant cells. Taken together, these findings reveal that TRIM24 plays a pivotal regulatory role in the crosstalk between the proteasome and autophagy in BTZ-resistant MCL cells by modulating ubiquitin chain abundance, thereby influencing the activation of one or the other proteolytic pathway.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"108"},"PeriodicalIF":6.1,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11914149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647339","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}