Apoptosis最新文献

{"title":"Copper homeostasis and cuproptosis in cancer: mitochondrial metabolic dependency and nanomedicine-based therapeutic strategies","authors":"Xuan Han,&nbsp;Zeyu Peng,&nbsp;Keying Cao,&nbsp;Gaofeng Liang","doi":"10.1007/s10495-026-02352-9","DOIUrl":"10.1007/s10495-026-02352-9","url":null,"abstract":"<div><p>Copper (Cu), as an essential trace element, is involved in a variety of key biological processes, such as mitochondrial respiratory chain, antioxidant defense, and cellular signal transduction. It is also potentially toxic while maintaining life activities: once intracellular free copper increases or becomes imbalanced, it may trigger a cascade of stress responses, including protein misfolding, disruption of redox homeostasis, and mitochondrial dysfunction. Therefore, the body maintains copper homeostasis through fine-tuned uptake, transport, storage, and efflux systems, ensuring copper remains in dynamic balance. Tumor cells often undergo adaptive changes in metal ion homeostasis in response to metabolic reprogramming and microenvironmental selective pressures. Abnormal copper metabolism has been considered closely related to tumor development, invasion, metastasis, and treatment tolerance. In recent years, cuproptosis has provided a new theoretical framework for studying the relationship between copper and tumors. Our manuscript expounds on the therapeutic value of copper and cuproptosis in tumor progression and treatment, providing a new entry point for updating accurate cancer treatment strategies.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257005","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}

{"title":"Zinc regulates the balance of specific gut microbiota through MTF1/Nrf2 and mitigates ferroptosis through activation of PINK1/Parkin/mitophagy via the gut-kidney axis in sepsis-associated acute kidney injury in pregnant mice","authors":"Xingfeng Cheng,&nbsp;Yang Chen,&nbsp;Di Meng,&nbsp;Jie Ren,&nbsp;Xiaolong Yu,&nbsp;Huizhen Wang,&nbsp;Jun Guo","doi":"10.1007/s10495-026-02353-8","DOIUrl":"10.1007/s10495-026-02353-8","url":null,"abstract":"<div><p>This research intends to explore the molecular mechanism by which Zn alleviates septic AKI in pregnant mice, with a focus on the gut-kidney axis. A septic AKI model was established in non-pregnant and pregnant mice using the cecal ligation and puncture (CLP) method. The changes in serum Zn over time after modeling were observed. Mice were administered with varying doses (low, medium, and high) of zinc gluconate <i>via</i> gavage, subjected to MTF1 knockdown or overexpression, or treated with the PINK1 activator PARL-IN-2, the autophagy inhibitor chloroquine, or the ferroptosis inhibitor Ferrostatin-1. Following these interventions, pathological changes in kidney and intestinal tissues, intestinal barrier function, abundance of specific gut microbiota, and mitophagy and ferroptosis in kidney tissues were assessed accordingly. In CLP-induced septic pregnant mice, serum Zn was depleted. These changes coincided with significant pathological changes in kidney tissue, the intestinal barrier disruption, dysbiosis of the specific gut microbiota, repressed mitophagy, and enhanced ferroptosis. Zn treatment partially ameliorated the kidney injury, activated the MTF1/Nrf2 pathway, restored intestinal barrier function and specific gut microbiota abundance, activated PINK1/Parkin and mitophagy, and restrained ferroptosis. Mechanistic experiments validated that Zn could activate the MTF1/Nrf2 axis, restore the balance of specific gut microbiota abundance, and activate PINK1/Parkin/mitophagy through the gut-kidney axis to alleviate ferroptosis and ameliorate septic AKI in pregnant mice. Zinc ameliorates sepsis-induced AKI in pregnant mice by activating PINK1/Parkin-mediated mitophagy through the MTF1/Nrf2–gut–kidney axis, thereby alleviating ferroptosis and preserving kidney function.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257021","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}

{"title":"Programmed cell death and metastatic evolution in breast cancer: the role of anoikis, necroptosis, and ferroptosis","authors":"Alireza H. Shirvani,&nbsp;Shirin Mohammadian,&nbsp;Shaghayegh Jamshidi,&nbsp;Mohammad H. Khodabandehloo,&nbsp;Soheila Zangoie,&nbsp;Romisa S. Moghadam,&nbsp;Adel Amoozade,&nbsp;Cena Aram,&nbsp;Mona Rahimi,&nbsp;Mohammad Javad Kamali,&nbsp;Ali Alishvandi","doi":"10.1007/s10495-026-02375-2","DOIUrl":"10.1007/s10495-026-02375-2","url":null,"abstract":"<div><p>Metastatic breast cancer (MBC) remains the leading cause of breast cancer–related mortality, driven by the ability of disseminated tumor cells to survive a series of intrinsically lethal stresses encountered during systemic progression, including loss of extracellular matrix attachment, oxidative damage, and immune-mediated cytotoxicity. While resistance to apoptosis has long been considered central to tumorigenesis, it is now evident that metastatic competence depends on coordinated modulation of multiple regulated cell death (RCD) pathways, notably anoikis, necroptosis, and ferroptosis. In this review, we synthesize current mechanistic and translational evidence describing how breast cancer cells reprogram these pathways across the metastatic cascade. We first delineate the molecular basis of anoikis and the adaptive mechanisms that enable anchorage-independent survival. We then examine how circulating tumor cells withstand oxidative and inflammatory stress through redox adaptation and modulation of necroptotic signaling. Within distant organ niches, microenvironmental factors—including metabolic constraints, inflammatory cues, and iron availability—govern susceptibility to ferroptosis and necroptosis, thereby influencing dormancy and metastatic outgrowth. We further introduce the concept of cell death plasticity, defined as the dynamic and context-dependent capacity of tumor cells to modulate, switch between, or simultaneously regulate multiple RCD pathways in response to microenvironmental and therapeutic pressures. This adaptive property underlies both metastatic persistence and therapy resistance, while simultaneously generating context-specific vulnerabilities. Finally, we critically evaluate emerging therapeutic strategies and biomarker frameworks aimed at exploiting these vulnerabilities. Despite strong preclinical rationale, clinical translation remains limited, underscoring the need for biomarker-driven and combinatorial approaches. Collectively, understanding the dynamic interplay among RCD pathways provides a conceptual and translational foundation for targeting metastatic and treatment-resistant breast cancer.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 7","pages":""},"PeriodicalIF":9.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148256973","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}

{"title":"A novel ZNF263-SMOX-ROS-TRIB3 signaling axis drives Wnt/β-catenin activation and metastatic progression in colorectal cancer","authors":"Longhe Sun,&nbsp;Youlei Zhang,&nbsp;Xianhu Zhang,&nbsp;Jiajie Zhou,&nbsp;Lili Ji,&nbsp;Ruiqi Li,&nbsp;Shuai Zhao,&nbsp;Yayan Fu,&nbsp;Jie Wang,&nbsp;Min Tang,&nbsp;Wei Wang,&nbsp;Chunhua Qian,&nbsp;Qiannan Sun,&nbsp;Daorong Wang","doi":"10.1007/s10495-026-02359-2","DOIUrl":"10.1007/s10495-026-02359-2","url":null,"abstract":"<div><p>Spermine oxidase (SMOX), a key enzyme in polyamine catabolism, has been increasingly linked to tumor progression. However, its regulatory network and biological significance in colorectal cancer (CRC), particularly in metastasis, remain largely undefined. Integrated transcriptomic analyses of CRC peritoneal metastasis samples, GEO datasets, and TCGA cohorts were performed to determine SMOX expression and prognostic value. Functional assays in vitro and xenograft/peritoneal metastasis models in vivo were used to assess the impact of SMOX knockdown or overexpression. Mechanistic studies included pathway enrichment, Western blotting, Co-IP, and ChIP-qPCR. SMOX was consistently upregulated in CRC tissues and cell lines, and high SMOX expression correlated with advanced stage, lymphatic metastasis, and unfavorable prognosis. Functionally, SMOX depletion markedly suppressed CRC cell proliferation, colony formation, migration, and invasion, and impaired tumor growth and peritoneal dissemination in vivo; SMOX overexpression exerted opposite protumorigenic effects. Mechanistically, SMOX elevated intracellular ROS levels, leading to transcriptional upregulation of the pseudokinase TRIB3. TRIB3 interacted with and suppressed GSK-3β activity, consequently stabilizing β-catenin and activating the Wnt/β-catenin pathway. Moreover, we identified ZNF263 as a previously unrecognized transcriptional activator of SMOX; ZNF263 directly bound to the SMOX promoter and drove its overexpression in CRC. Together, these findings delineate a novel “ZNF263–SMOX–ROS–TRIB3–GSK-3β–β-catenin” axis. Our study reveals SMOX as a critical driver of CRC progression and metastasis through ROS-mediated TRIB3 induction and subsequent Wnt/β-catenin activation, under the upstream regulation of ZNF263. This signaling axis provides new mechanistic insights and highlights SMOX/TRIB3 as promising therapeutic targets in CRC.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10495-026-02359-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148203850","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 programmed cell death: a novel therapeutic paradigm for cancer based on mode-of-death classification","authors":"Xi Qiao,&nbsp;Ting Ye,&nbsp;Tinggai Wu,&nbsp;Xu Han,&nbsp;Tiantian Sun,&nbsp;Haiqiang Wang,&nbsp;Junru Jia,&nbsp;Yuanyuan Dai,&nbsp;Ruohan Yun,&nbsp;Shuo Jiang,&nbsp;Yuming Qin,&nbsp;Zhenzhen Liu,&nbsp;Yang An,&nbsp;Xinying Ji,&nbsp;Shuangyu Lv","doi":"10.1007/s10495-026-02324-z","DOIUrl":"10.1007/s10495-026-02324-z","url":null,"abstract":"<div><p>Programmed cell death (PCD) refers to a form of cell death governed by genetic regulation, and consists of several distinct pathways, including apoptosis, autophagy, cuproptosis, ferroptosis, necroptosis, paraptosis and pyroptosis. These pathways are crucial for maintaining intracellular stability and homeostasis, which are involved in the pathogenesis of various diseases. This review innovatively proposes an integrated framework classified by death patterns, and systematically expounds the strategic significance of targeting PCD in cancer treatment. Based on this framework, we conduct an in-depth analysis of how to design corresponding therapeutic strategies for different death patterns, with a particular emphasis on the complex cross-talk and synergistic effects among different PCD pathways. Moreover, we demonstrate that this interaction is the cornerstone for designing the next generation of combination treatment regimens. The aim is to lay a foundation and point out the future direction for the development of more effective and targeted cancer treatment strategies based on the regulation of PCD networks.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197158","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}

{"title":"Targeted delivery of IDR-1018 via biomimetic magnetic nanovesicles suppresses neurovascular cell death and promotes angiogenic repair after neonatal hypoxic-ischemic brain injury","authors":"Jing Zhao,&nbsp;Daoxin Liang,&nbsp;Maoting Xiong,&nbsp;Jiahong Deng,&nbsp;Lihong Hu,&nbsp;Lin Jiang,&nbsp;Can Yang","doi":"10.1007/s10495-026-02357-4","DOIUrl":"10.1007/s10495-026-02357-4","url":null,"abstract":"<div><p>Neonatal hypoxic-ischemic brain damage (HIBD) is characterized by severe endothelial injury, inflammation, and apoptosis, which together contribute to irreversible neurodevelopmental deficits. In this study, we developed a biomimetic magnetic nanovesicle platform (IDR-MNC@RMVs) loaded with the host defense peptide IDR-1018 as a targeted therapeutic strategy for neonatal HIBD. Under external magnetic guidance, IDR-MNC@RMVs preferentially accumulated in ischemic brain regions, where they markedly reduced neuronal and vascular injury, attenuated brain atrophy, and improved neurological recovery in neonatal mice. Mechanistically, integrated analyses using single-cell RNA sequencing, transcriptomics, and functional assays showed that IDR-MNC@RMVs enhanced endothelial survival and angiogenic activity through activation of the ITGB3/VEGFA signaling axis. In vitro, IDR-MNC@RMVs protected hypoxia-injured human brain microvascular endothelial cells by restoring proliferation and migration while reducing apoptosis, whereas these protective effects were largely abolished after ITGB3 knockdown. In vivo, histological analyses further indicated reduced inflammatory injury and improved vascular preservation after treatment. Collectively, these findings identify IDR-MNC@RMVs as a promising nanotherapeutic strategy that promotes vascular repair and tissue recovery after neonatal hypoxic-ischemic injury. This work highlights the potential of combining biomimetic nanotechnology with peptide-based therapy for neonatal brain injury.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142263","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}

{"title":"Succinate drives breast cancer bone metastasis by activating the HIF1α/YTHDF1/YAP signaling axis to upregulate chemokine CXCL5 and disrupt the bone microenvironment","authors":"Jiao Xue,&nbsp;Chunhui Zhu,&nbsp;Yatao Zhai,&nbsp;Weixian Chen,&nbsp;Jianbo Dai,&nbsp;Dong Zheng,&nbsp;Rui Geng","doi":"10.1007/s10495-026-02361-8","DOIUrl":"10.1007/s10495-026-02361-8","url":null,"abstract":"<div><p>This study aimed to clarify how the metabolite succinate contributes to breast cancer (BC) bone metastasis by upregulating the chemokine CXCL5, mediated through the HIF1α/YTHDF1/YAP signaling pathway, ultimately altering the bone microenvironment. A murine bone metastasis model was established using 4T1 BC cells. Tumor progression and osteolysis were monitored via in vivo imaging (IVIS) and micro-computed tomography (micro-CT). Integrated metabolomics and RNA-seq analyses identified key alterations. The proposed signaling axis was validated using Western blot, RT-qPCR, Chromatin Immunoprecipitation (ChIP-qPCR), m6A RNA immunoprecipitation (MeRIP-qPCR), and luciferase reporter assays. Macrophage polarization was analyzed by flow cytometry. Functional impacts on bone cells were assessed using osteoblast mineralization and osteoclast tartrate-resistant acid phosphatase (TRAP) staining assays. Metabolomic profiling revealed significant succinate enrichment. Succinate activated HIF1α via its receptor SUCNR1. HIF1α transcriptionally upregulated YTHDF1, which subsequently stabilized YAP mRNA via an m6A-dependent mechanism. YAP directly bound to the CXCL5 promoter, enhancing its expression. In vitro, succinate-induced CXCL5 promoted tumor-associated macrophage (TAM) polarization, inhibited osteoblast function, and activated osteoclasts. In vivo, succinate-treated mice exhibited enhanced bone metastasis, severe osteolysis, elevated serum CTX-I, and reduced OCN levels. Succinate drives BC bone metastasis by activating the HIF1α/YTHDF1/YAP/CXCL5 axis, which reprograms the bone microenvironment. This study reveals a novel metabolic-inflammatory-bone niche interplay, identifying CXCL5 as a potential therapeutic target.</p><h3>Graphical abstract</h3><p>Schematic illustration showing that succinate promotes breast cancer bone metastasis by activating the HIF1α/YTHDF1/YAP axis to upregulate CXCL5 and accelerate inflammatory remodeling of the bone microenvironment</p><div><figure><div><div><picture><source><img></source></picture><span>The alternative text for this image may have been generated using AI.</span></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142341","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}

{"title":"Differential distribution of microplastics in breast cancer and peritumoral tissues and relationship with clinical characteristics","authors":"Bei Sun,&nbsp;Jinpu Liu,&nbsp;Xinyi Wen,&nbsp;Dongzhi Hu,&nbsp;Zhanhua Gao,&nbsp;Minghan Qiu,&nbsp;Shoujun Wang,&nbsp;Zhansheng Jiang,&nbsp;Mingqing Zhang,&nbsp;Chong Chen,&nbsp;Haiyang Zhang,&nbsp;Feng He,&nbsp;Jie Hao","doi":"10.1007/s10495-026-02372-5","DOIUrl":"10.1007/s10495-026-02372-5","url":null,"abstract":"<div><p>The distribution characteristics of microplastics (MPs) in paired breast cancer tumor and para-tumor tissues, and their potential associations with clinical characteristics, remain insufficiently understood. This study included eight breast cancer patients with surgical resection whose paired tumor and para-tumor tissues were collected. The morphologies, particle sizes, and types of microplastics within the tissues were identified and characterized using Laser Direct Infrared (LDIR) spectroscopy and Scanning Electron Microscopy (SEM). Moreover, correlations between microplastic abundance and patients’ demographic and clinical characteristics were analyzed. SEM imaging revealed diverse morphologies—granular, fibrous, and irregular—often exhibiting folds and fractures. The majority of microplastic particles were within the 20–100 μm size range. Multiple types of polymeric microplastics—including Fluororubber (Flu), polyethylene (PE), polyethylene terephthalate, polypropylene, and polyvinyl chloride (PVC)—were detected in all paired samples. Notably, the abundance of Flu, PE, and PVC was significantly higher in tumor tissues compared to para-tumor tissues. Correlation analyses identified exploratory associations between selected microplastic types, body mass index, and certain tumor biomarkers. These findings provide preliminary evidence of tissue-specific MP distribution in breast cancer and support further investigation into the potential biological relevance of microplastics in breast cancer.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148247","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}

{"title":"Total flavones of Rhododendron protect against BBB injury following cerebral ischemia/reperfusion via promoting astrocytic polarization towards A2 subtype","authors":"Xin Xu,&nbsp;Ziyu Wang,&nbsp;Falan Hu,&nbsp;Leshu Wang,&nbsp;Baoyun Guo,&nbsp;Ziyan Li,&nbsp;Jinhua Chen,&nbsp;Jiyue Wen","doi":"10.1007/s10495-026-02343-w","DOIUrl":"10.1007/s10495-026-02343-w","url":null,"abstract":"<div><p>This study investigates the role and underlying mechanisms of total flavones of <i>Rhododendron</i> (TFR) in blood-brain barrier (BBB) disruption following transient bilateral common carotid artery occlusion-induced cerebral ischemia/reperfusion (I/R), focusing on whether A2 astrocyte polarization mediates the protective effects of TFR. RNA sequencing analysis was performed to elucidate the molecular mechanisms underlying the differential effects of A1 and A2 astrocytes on endothelial function. TFR treatment significantly reduced Evans blue (EB) extravasation and attenuated the downregulation of claudin-5, ZO-1, occludin, and CD31 in mouse hippocampal tissues. Furthermore, TFR enhanced the production and release of cystathionine-β-synthase (CBS)-derived H₂S from astrocytes. Both TFR and TFR-induced A2 astrocytes promoted the expression of tight junction proteins in endothelial cells (ECs) following oxygen-glucose deprivation/reoxygenation (OGD/R). RNA sequencing revealed upregulation of Caspase-11 in A1 astrocytes and downregulation in A2 astrocytes. Moreover, A1 astrocytes exhibited increased expression of matrix metalloproteinase (MMP)-9 and TNF-α, whereas A2 astrocytes showed elevated levels of IL-10. Collectively, these findings indicate that TFR mitigates BBB disruption after cerebral I/R through dual mechanisms: directly upregulating tight junction proteins in brain microvascular endothelial cells and indirectly promoting astrocyte polarization toward the A2 subtype, which is associated with reduced Caspase-11 expression, enhanced IL-10 secretion, and increased CBS-derived H₂S production.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148100918","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}

{"title":"The dark side of apoptosis: how dying cells fuel tumor angiogenesis","authors":"Nivedha Varadharajan,&nbsp;Vimalraj Selvaraj","doi":"10.1007/s10495-026-02371-6","DOIUrl":"10.1007/s10495-026-02371-6","url":null,"abstract":"","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052041","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}