APOPTOSIS细胞凋亡
APOPTOSIS(英文缩写 APOPTOSIS),ISSN 1360-8185,eISSN 1573-675X,中文译名:细胞凋亡 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.561 | Q2 |
| 2022 | 7.200 | Q1 |
| 2023 | 6.100 | Q1 |
| 2024 | 8.100 | Q1 |
| 2025 | 9.000 | Q1 |
APOPTOSIS 最新收录文献
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1. Ru3: a novel ruthenium-based compound overcomes cisplatin resistance in non-small cell lung cancer via the E2F2-IGFBP3-GPX4 pathway.
1. Ru3：一种新型钌基化合物通过E2F2-IGFBP3-GPX4通路克服非小细胞肺癌的顺铂耐药性PMID:日期:2026-10-03Cisplatin resistance remains a major hurdle in non-small cell lung cancer (NSCLC) treatment. Here, we designed and synthesized a novel ruthenium-based compound, which selectively kills cisplatin-resistant NSCLC cells while sparing parental cells. Mechanistically, Ru3 triggers mitochondrial damage and reactive oxygen species (ROS) accumulation. In addition, it upregulates the transcription factor E2F2, which directly represses IGFBP3 expression. IGFBP3 normally scavenges ROS via the GPX4 system; thus, E2F2-mediated IGFBP3 suppression disrupts this antioxidant defense, exacerbating ROS levels and cell death. Notably, cisplatin-resistant cells exhibit elevated GPX4 and IGFBP3 expression, making them particularly vulnerable to Ru3. This study elucidates the E2F2-IGFBP3-GPX4 axis as a novel therapeutic vulnerability and highlights Ru3 as a promising agent for refractory NSCLC.
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2. The ferroptosis-cuproptosis crosstalk in hematological malignancies: multi-omics insights into gene-regulated cell death and emerging therapeutic opportunities.
2. 血液系统恶性肿瘤中铁死亡与铜死亡的交互作用：多组学视角下基因调控的细胞死亡及新兴治疗机遇PMID:日期:2026-10-03The broadening field of regulated cell death (RCD) has shown a complex, intertwined web of pathways that are not confined to apoptosis but also to ferroptosis, cuproptosis, necroptosis, and other non-canonical mechanisms, especially in haematological malignancies (HMs). Out of these, ferroptosis and cuproptosis stand out as metabolic-based forms of death that are regulated by iron-dependent and copper-dependent processes, respectively. This review presents the notion of a single ferroptosis-cuproptosis axis, a Metallo-redox network that encompasses lipid peroxidation, mitochondrial dysfunction, and proteotoxic stress to control cell fate decisions. We underscore the fact that haematological cancers use metal ion flux, redox homeostasis, and metabolic plasticity to bypass apoptosis, but are susceptible to other RCD pathways. This work, based on multi-omics methods, such as genomics, transcriptomics, proteomics, metabolomics, and metal omics, describes how integrative modelling can unravel RCD susceptibility landscapes and discover context-specific therapeutic targets. The single-cell and spatial analyses further demonstrate intra-tumoral heterogeneity and switching between death pathways in response to therapeutic pressure. New treatment options that are being developed to address this axis such as ferroptosis inducers, copper ionophores, and complex nanomedicine systems with the ability to deliver therapeutics and modify pathways. The review also covers such challenges of translation as the lack of standardization of biomarkers, clinical trial design, and dynamic stratification of patients. Lastly, suggest an outlook system combining artificial intelligence, synthetic biology, and organoid-based systems to permit precision cell death engineering. Together, this literature makes the ferroptosis-cuproptosis axis a novel change in the outlook of future therapies in haematological cancers.
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3. Metabolic vulnerabilities in multiple myeloma: targeting iron and amino acid metabolism to induce ferroptosis.
PMID:日期:2026-10-03Could ferroptosis, a novel cell death pathway, offer a potential therapeutic strategy for multiple myeloma (MM)? Our previous research showed that ferroptosis is suppressed in MM patients, with varying sensitivities among MM cells. In this study, metabolomic analysis highlighted the pivotal role of amino acid metabolism, rather than lipid metabolism, in determining MM cells' sensitivity to ferroptosis. We further analyzed iron metabolism, another key factor influencing ferroptosis sensitivity, by collecting peripheral blood samples from 120 MM patients. Our analysis revealed a significant reduction in the levels of transferrin (TF), an essential iron-transporting protein. Moreover, low TF levels were associated with significantly worse progression-free survival and overall survival. Erastin treatment together with TF supplementation markedly enhanced ferroptosis in MM cells in vitro and in xenograft models. MM cells suppressed TF secretion by monocytes in the bone marrow microenvironment, contributing to the decreased TF levels in MM patients. The transcription factor CEBPB, found in MM cell-derived extracellular vesicles, plays a key role in this process. In conclusion, Our findings identify amino acid metabolism and iron metabolism as distinct metabolic features associated with ferroptosis sensitivity in MM. Ferroptosis, induced by erastin and TF, holds promise as a potential therapeutic strategy for MM and provides new insights for developing more effective therapies.
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4. The role of lysosome-dependent cell death in cancer.
4. 溶酶体依赖性细胞死亡在癌症中的作用PMID:日期:2026-10-03Lysosome-dependent cell death (LDCD) is a distinct mode of regulated cell death, which differs from canonical cell death pathways such as apoptosis and necrosis. Its key features include lysosomal membrane permeabilization and the downstream signaling cascades triggered by cathepsin release. Recent studies have demonstrated that LDCD exerts dual, intricate influences on cancer initiation, progression, immune homeostasis and therapeutic responses. It not only confers a survival advantage upon cancer cells but also represents a promising target for targeted antitumor therapy. This review systematically summarizes the molecular mechanisms underlying LDCD, its dual regulatory roles in cancer, and LDCD-based anticancer therapeutic strategies, and outlines future research directions. Ultimately, this work sheds light on the mechanistic link between LDCD and oncogenesis, providing a rationale for the development of targeted antitumor strategies.
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5. Exploring regulated cell death in renal cell carcinoma: mechanistic insights and therapeutic perspectives.
5. 探索肾细胞癌中的调节性细胞死亡：机制见解与治疗前景PMID:日期:2026-10-03Renal cell carcinoma (RCC) is the third most prevalent urological malignancy, characterized by histological heterogeneity and complex molecular landscapes. Although established regimens, including surgical intervention, targeted therapies and immunotherapy, effectively manage early-stage disease, patients with advanced RCC still have a poor prognosis. The expanding spectrum of regulated cell death (RCD), ranging from established apoptosis and ferroptosis to emerging modalities like cuproptosis, disulfidptosis and ammonia-induced cell death, offers novel mechanistic insights into tumor vulnerabilities. This tumor progression and subsequent therapeutic resistance are substantially mediated by dysregulated networks of RCD. To systematically deconstruct this mechanistic complexity, this review stratifies RCD into three specific functional dimensions: precise protein signaling, intracellular homeostasis dysregulation, and physiological dysfunction. Because RCC intrinsically evades cascade-governed pathways such as apoptosis to survive immune elimination, its inherent metabolic reprogramming concomitantly creates paradoxical vulnerabilities. Consequently, these tumors exhibit profound susceptibility to homeostasis-disrupting modalities like ferroptosis, cuproptosis, disulfidptosis, and ammonia-induced cell death. Extending this mechanistic framework beyond clear cell RCC (ccRCC), we define the unique metabolic and redox dependencies of underrepresented non-clear cell variants, including papillary RCC (pRCC), chromophobe RCC (chRCC), fumarate hydratase (FH)-deficient RCC and TFE3-rearranged RCC. By evaluating current RCD-targeted pharmacological interventions, this review highlights critical opportunities to exploit these functional dependencies, offering rational approaches to overcome intrinsic resistance and complement existing therapies. Ultimately, integrating this multidimensional RCD framework with multi-omics profiling facilitates a deeper biological understanding of renal tumors and provides a necessary foundation to accelerate the development of precision oncology.
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6. Anastasis: an unwelcome guest in cancer therapy.
6. 阿纳斯塔西斯：癌症治疗中不受欢迎的客人PMID:日期:2026-10-03Anastasis is a newly identified cellular recovery process that enables cells to regain viability after progressing into execution-phase apoptosis. In cancer, this process may allow tumor cells to survive transient cytotoxic stress and subsequently acquire more aggressive phenotypes, including enhanced migration, invasion, and resistance to therapy. Although anastasis has attracted increasing attention, its biological significance and contribution to cancer progression remain incompletely understood. In this review, we summarize the defining features and biological processes of anastasis and critically evaluate current evidence linking post-apoptotic recovery to cancer-associated phenotypes, including apoptosis regulation, metastasis, angiogenesis, oxidative-stress adaptation, and epithelial-mesenchymal transition. We further discuss molecular pathways implicated in anastatic recovery and examine potential therapeutic strategies aimed at limiting post-apoptotic survival in cancer cells. Finally, we highlight major challenges in the field, including the need for more specific biomarkers, physiologically relevant in vivo models, and direct clinical validation, and outline key unresolved questions that should guide future investigation.
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7. The role of vitamin D signalling in β cell apoptosis: a systematic review.
7. 维生素D信号在β细胞凋亡中的作用：一项系统综述PMID:日期:2026-10-01Vitamin D signalling, primarily through the vitamin D receptor (VDR), regulates cellular survival and programmed cell death. This systematic review aims to synthesise current evidence on the role of vitamin D in pancreatic β-cell apoptosis. Medline, Embase, and Scopus were searched for original studies investigating vitamin D, vitamin D analogues, or VDR-related interventions in experimental models of β-cell apoptosis or programmed cell death. 26 studies were included. Across in vitro, ex vivo, and in vivo models, vitamin D signalling protected β-cells against apoptosis induced by cytokine-mediated inflammation, oxidative stress, glucotoxicity, lipotoxicity, streptozotocin exposure, and diabetic stress. These effects were associated with reduced NF-κB signalling, nitric oxide and reactive oxygen species production, improved mitochondrial stability, modulation of Bcl-2 family proteins, inhibition of endoplasmic reticulum stress, and regulation of pyroptosis, ferroptosis, and autophagy-related survival mechanisms. VDR activation also supported β-cell identity, insulin secretion, and β-cell mass preservation. In contrast, calcitriol-associated growth inhibition and increased apoptosis were reported in βTC insulinoma models. Vitamin D signalling generally appears cytoprotective in β-cells exposed to inflammatory, oxidative, and metabolic stress. However, its effects on β-cell survival are model- and context-dependent, reflecting differences in cellular background, experimental stressors, and methods used to assess cell death.
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8. The emerging roles of disulfidptosis in cancer.
8. 二硫死亡在癌症中的新作用PMID:日期:2026-09-23Cancer persists as a significant global health burden, with conventional therapeutic approaches frequently constrained by drug resistance and disease relapse, underscoring the urgent requirement for innovative treatment modalities. Recent advances in regulated cell death have uncovered promising therapeutic avenues for cancer. Amidst these newly identified processes, disulfidptosis-a distinct type of programmed cell death triggered by disulfide stress-has garnered significant attention because of its specific metabolic reliance. The underlying mechanism centers on pathological intracellular cystine accumulation coupled with depletion of NADPH reducing equivalents, stemming from elevated levels of the cystine transporter SLC7A11 during metabolic stress states such as glucose deprivation. This cascade induces aberrant disulfide bonding followed by actin cytoskeleton disruption, ultimately resulting in cellular demise. Evidence suggests that disulfidptosis-related genes exhibit altered expression across various malignancies, including lung, liver, and colorectal cancers, and are strongly correlated with disease progression and patient outcomes. Prognostic models constructed based on bioinformatics not only demonstrate good predictive efficacy but also reflect characteristics of the tumor immune microenvironment. This process reveals a fundamental weakness in cancer cells after metabolic reprogramming, establishing the induction of disulfidptosis via SLC7A11 inhibition or modulation of associated metabolic pathways as a promising new anticancer approach. It also provides a rationale for combination strategies with chemotherapy, targeted therapy, and immunotherapy. Nonetheless, its interaction with different cell death mechanisms (including ferroptosis), the variability observed across various cancer types, and the translation to clinical applications remain significant challenges and key avenues for future investigation.
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9. SUCLG2 contributes to platinum resistance in lung adenocarcinoma through enhancing succinylation of GAC and glutamine metabolism.
PMID:日期:2026-09-23Platinum-based drugs constitute first-line chemotherapy for lung adenocarcinoma (LUAD), yet resistance emerges in 50-70% of patients, representing a major clinical challenge. Synthetase GDP-forming subunit β (SUCLG2), the beta subunit of succinyl-CoA synthetase, is a key enzyme in the tricarboxylic acid (TCA) cycle. Using untargeted proteomic profiling, we identified SUCLG2 as a potential contributor of platinum resistance in LUAD. Further knockout of SUCLG2 significantly enhanced cellular sensitivity to platinum-based drugs. Mechanistically, using targeted metabolomics, we found that SUCLG2 conferred platinum resistance by promoting glutamine metabolism and facilitating the succinylation of glutaminase (GAC). This post‑translational modification enhanced GAC activity, thereby reducing ROS generation and suppressing apoptosis in LUAD cells. SUCLG2 was found to be highly expressed in both LUAD tissues and platinum-resistant cell lines. Consistent with cellular findings, animal experiments confirmed that elevated SUCLG2 expression critically contributes to platinum resistance in vivo. Our findings provide new insights into the molecular mechanisms underlying platinum resistance in LUAD and suggest novel therapeutic strategies.
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10. GLG1 in cancer-associated fibroblasts promotes bladder cancer growth while limiting tumor apoptosis.
10. 癌症相关成纤维细胞中的GLG1促进膀胱癌生长，同时限制肿瘤凋亡PMID:日期:2026-09-23Cancer-associated fibroblasts (CAFs) shape bladder cancer progression, but functionally relevant CAF-associated drivers remain insufficiently characterized. This study aimed to identify CAF-enriched genes with translational relevance and to determine whether GLG1 mediates tumor-stromal crosstalk in bladder cancer. Single-cell RNA sequencing from bladder cancer tissues was integrated with Mendelian randomization, Bayesian colocalization, correlation analyses, immunostaining of clinical specimens, CAF-conditioned medium assays, GLG1 knockdown/overexpression, TGF-β1/Smad2/3 assessment, and xenograft modeling. Single-cell profiling of nine bladder cancer samples retained 60,561 cells and identified fibroblast-enriched transcriptional programs. Among 960 fibroblast-enriched genes, Mendelian randomization identified 22 genes whose genetically predicted expression was associated with bladder cancer risk, and colocalization prioritized GLG1, HES4, and HSP90B1. GLG1 was selected for validation because it showed fibroblast-enriched expression, genetic support for bladder cancer association, and shared cis-eQTL/GWAS signals. GLG1 expression was higher in tumor tissues than in adjacent normal tissues, consistent with a stromal localization pattern, and GLG1 positivity was associated with tumor invasiveness. Tumor-derived TGF-β1/Smad2/3 signaling contributed to GLG1 upregulation in fibroblasts. CAF-conditioned medium enhanced EJ-1 cell viability, migration, and Matrigel invasion; these effects were weakened by GLG1 silencing and strengthened by GLG1 overexpression in CAFs. In xenografts, CAFs-shGLG1 reduced tumor growth and Ki-67 positivity and increased TUNEL-positive tumor cells relative to CAFs-shNC, whereas CAFs-OE-GLG1 showed the opposite Ki-67 and TUNEL staining pattern. CAF-associated GLG1 promotes bladder cancer cell viability, migration, Matrigel invasion, and xenograft growth while limiting tumor-cell apoptosis, likely by reinforcing tumor-stromal crosstalk. These findings support GLG1 as a stromal factor involved in bladder cancer progression and provide a basis for further evaluation of its biomarker potential and therapeutic relevance.