Apoptosis最新文献

{"title":"Mitochondria–membrane contact duration: a spatial checkpoint for oxidative cell death","authors":"Qingfeng Wu, Qingbin Zhao","doi":"10.1007/s10495-026-02369-0","DOIUrl":"10.1007/s10495-026-02369-0","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":"148052083","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":"Metabolic inflexibility across heart failure phenotypes: mechanisms and type-specific therapeutic implications","authors":"Li Chen,&nbsp;Xin-Rui Yang,&nbsp;Yan Jiang,&nbsp;Shi-Qi Cheng,&nbsp;Zhen-Xun Wan,&nbsp;Jin-Wen Wu,&nbsp;Ming-Tai Chen,&nbsp;Yuan-Yuan Li,&nbsp;Gang Luo,&nbsp;Meng-Nan Liu","doi":"10.1007/s10495-026-02376-1","DOIUrl":"10.1007/s10495-026-02376-1","url":null,"abstract":"<div><p>Heart failure (HF) is a heterogeneous clinical syndrome characterized by phenotype-specific metabolic remodeling (e.g., ischemic vs. nonischemic, HF with HFrEF vs. HFpEF), with impaired metabolic flexibility serving as a central pathophysiological link. The physiological basis of normal cardiac metabolic flexibility is outlined, and the temporal trajectories and molecular mechanisms of metabolic remodeling across compensated, early decompensated, and end-stage HF are delineated. Key mechanisms, including dysregulated mitochondrial quality control, imbalanced substrate utilization, and transcriptional dysregulation are examined. Furthermore, multidimensional metabolic therapeutic strategies are summarized, and the translational potential of novel biomarkers (e.g., ketone bodies, acylcarnitines) is discussed. It is indicated the efficacy of metabolic therapies depends critically on HF phenotype, disease stage, and global metabolic network integrity. Future research is prioritized metabolomics-based precise phenotyping, dynamic monitoring of remodeling trajectories, and the development of systematic regulatory strategies featuring multi-target combinations and cardiac-specific delivery, so as to advance the clinical translation of metabolic therapies for HF.</p></div>","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":"148051936","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":"Metabolic regulation of ferroptosis in cancer: mechanisms, pharmacological inducers, and translational challenges","authors":"Yanfang Liu","doi":"10.1007/s10495-026-02377-0","DOIUrl":"10.1007/s10495-026-02377-0","url":null,"abstract":"<div><p>Resistance to traditional apoptosis remains a central obstacle in oncology, especially in tumors that survive chemotherapy, targeted therapy, or immune pressure by acquiring metabolic plasticity. Ferroptosis, a non-apoptotic form of regulated cell death driven by iron-dependent lipid peroxidation, offers a mechanistically distinct opportunity to eliminate these refractory malignant states. In this review, we organize the field around three metabolic layers that govern ferroptosis in cancer: mobilizable iron pools and Fenton chemistry, lipid remodeling and membrane oxidation, and the dynamic balance between reactive oxygen species generation and antioxidant buffering. Rather than treating ferroptosis as a universal opportunity across all tumors, we emphasize how these layers create context-dependent liabilities in therapy-resistant disease. We then connect these layers to clinically relevant tumor contexts, including drug-tolerant persister cells, hypoxic solid tumors, and antioxidant-addicted cancer populations. Particular emphasis is placed on why lysosomal iron activation, lipid-droplet buffering, GSH/GPX4/FSP1 plasticity, medicinal chemistry, and nanomedicine-enabled delivery now represent major turning points in the field. By integrating mechanistic depth with translational challenges such as biomarker selection, intratumoral drug delivery, tumor-state heterogeneity, and therapeutic-window control, this review provides a cancer-therapy-oriented framework for the precision deployment of ferroptosis rather than a purely descriptive summary of ferroptosis biology.</p></div>","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":"148051975","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":"H4K8 lactylation-mediated ferroptosis defense drives EGFR-TKI resistance in lung adenocarcinoma","authors":"Shuman Zhen,&nbsp;Yifan Gao,&nbsp;Jiaqi Wang,&nbsp;Jingyi Ren,&nbsp;Huanting Pei,&nbsp;Danjing Yin,&nbsp;Yandong Deng","doi":"10.1007/s10495-026-02374-3","DOIUrl":"10.1007/s10495-026-02374-3","url":null,"abstract":"<div><p>Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) remains a major clinical challenge in non-small cell lung cancer. Emerging evidence indicates that metabolic reprogramming and epigenetic alterations contribute to drug resistance, particularly through the evasion of ferroptosis, a regulated form of cell death characterised by lipid peroxidation. This study investigated the role of lactate-associated histone modifications in driving EGFR-TKI resistance. Resistant lung adenocarcinoma tissues and cell lines were analysed using transcriptomics, Cleavage Under Targets and Tagmentation (CUT&amp;Tag) profiling, and biochemical assays. Glycolytic activity, lactate accumulation, and ferroptosis-related lipid peroxidation were assessed, followed by genetic and pharmacological interventions and in vivo xenograft validation. Resistant cells exhibited enhanced glycolysis and lactate accumulation, with pathway analyses highlighting ferroptosis evasion as a key resistance-associated process. Consequently, histone H4 lysine 8 lactylation (H4K8la) was significantly elevated in resistant tissues and cells. Mechanistically, H4K8la was enriched at transcription start sites, particularly at the promoter of aldo-keto reductase family 1 member C1 (AKR1C1). This epigenetic modification profoundly suppressed ferroptosis and promoted drug resistance. Disrupting this H4K8la-AKR1C1 defence axis restored lipid peroxidation, increased ferroptotic sensitivity, and resensitised resistant cells to EGFR-TKIs, as confirmed in vivo. These findings reveal a novel lactate-driven epigenetic mechanism that orchestrates ferroptosis escape and EGFR-TKI resistance, offering a promising therapeutic strategy to overcome treatment failure.</p></div>","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":"148052005","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":"Cholesterol as a metabolic integrator of oncogenic signaling, immune evasion, and therapy resistance","authors":"Vladislav Skossyrskiy,&nbsp;Evgeniy Prozorenko,&nbsp;Igor Gadaev,&nbsp;Andrey Skossyrskiy,&nbsp;Ekaterina Orlova,&nbsp;Marina Sekacheva","doi":"10.1007/s10495-026-02351-w","DOIUrl":"10.1007/s10495-026-02351-w","url":null,"abstract":"<div><p>Cholesterol is increasingly recognized as a central coordinator of tumor signaling, metabolism, and immune evasion. In addition to their structural role in membranes, cholesterol-enriched lipid rafts stabilize oncogenic pathways such as those involving EGFR, Src, and ERRα, promoting cancer stemness and therapeutic resistance. Excess cholesterol within mitochondria reduces membrane permeability, prevents cytochrome c release, and contributes to resistance to apoptosis. Moreover, cholesterol-derived oxysterols reshape the tumor microenvironment by inducing Th17 polarization, XBP1-dependent CD8⁺ T-cell exhaustion, and macrophage M2 reprogramming. These interconnected mechanisms reveal that cholesterol is a metabolic hub linking intracellular survival pathways with immune dysfunction. Pharmacologic and dietary modulators: Statin, ezetimibe, and ω-3 fatty acids can remodel cholesterol pools, reverse raft stabilization, and partially restore sensitivity to targeted or immune therapies in preclinical models. Recognizing cholesterol metabolism as a contributing factor to oncogenic signaling and immune suppression highlights potential theoretical avenues for biomarker-guided treatment combinations. This integrative framework positions cholesterol not only as a structural lipid but also as a dynamic regulator of tumor evolution and therapy response.</p></div>","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":"148052025","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":"Osteopontin-driven TGF-β1 signaling via integrin αvβ3-NF-κB axis impairs NK cell function in head and neck squamous cell carcinoma","authors":"Zhe Shen,&nbsp;Xin Li,&nbsp;Shi Luo,&nbsp;Yuzhang Gao,&nbsp;Imadoudini Hassimi Safia,&nbsp;Jie Jiang,&nbsp;Xin Qi,&nbsp;Wei Huang,&nbsp;Yalan Liu,&nbsp;Xing Fang,&nbsp;Yaoyun Tang,&nbsp;Ping Wu","doi":"10.1007/s10495-026-02333-y","DOIUrl":"10.1007/s10495-026-02333-y","url":null,"abstract":"<div><p>In head and neck squamous cell carcinoma (HNSCC), an immunosuppressive tumor microenvironment (TME) frequently leads to natural killer (NK) cell dysfunction, but the molecular mechanisms underlying this impairment remain unclear. Here, we combined flow cytometry and multiplex immunohistochemistry to evaluate NK cells infiltration and functional status in HNSCC tumors. Bulk RNA-seq datasets from patient cohorts and single-cell RNA-seq data were analyzed to identify transcriptional correlates of NK cells dysfunction. Mechanistic studies in tumor cell lines assessed the role of osteopontin (OPN)-integrin αvβ3/NF-κB signaling in modulating TGF-β1 production and its effects on NK cell activity. NK cells in HNSCC tumors exhibited reduced infiltration and diminished activation marker expression, coinciding with high OPN levels in the TME. Transcriptomic analyses demonstrated a strong inverse correlation between tumor SPP1 (encoding OPN) expression and NK cells abundance. Mechanistically, tumor-derived OPN engaged integrin αvβ3 to activate NF-κB signaling, inducing robust TGF-β1 secretion that suppressed NK cell activation and cytotoxic function. Single-cell RNA-seq analysis further confirmed the exhausted functional states of NK cells within the HNSCC TME. Tumor-derived OPN promotes immune evasion in HNSCC by driving TGF-β1-mediated suppression of NK cell activity. These findings highlight the OPN-TGF-β1 axis as a potential therapeutic target for restoring NK cell-mediated immunity in HNSCC.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148009355","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 pH-responsive silver nanoparticle platform overcomes MEK inhibitor resistance in neurofibroma via triacsin C-mediated lipid metabolic reprogramming","authors":"Jiang Xu,&nbsp;Longyan Liu,&nbsp;Shuheng Liu,&nbsp;Zesong He,&nbsp;Wei Meng","doi":"10.1007/s10495-026-02344-9","DOIUrl":"10.1007/s10495-026-02344-9","url":null,"abstract":"<div><p>To overcome resistance to MEK inhibitors such as selumetinib in neurofibroma, we developed a metabolism-targeted nanotherapeutic based on a pH-responsive silver nanoparticle platform (AgNP-PEG-TC) for delivering Triacsin C (TC), an inhibitor of long-chain acyl-CoA synthetases, to disrupt tumor-associated lipid metabolism. AgNP-PEG-TC was synthesized and characterized for its physicochemical properties, drug-loading efficiency, and pH-responsive release behavior. Its antitumor effects were assessed in human neurofibroma cells, including selumetinib-resistant cells, and in normal Schwann cells by examining proliferation, apoptosis, migration, and invasion. In vivo therapeutic efficacy and biosafety were evaluated in neurofibroma xenograft models. Bulk RNA sequencing, lipidomics, and protein analyses were performed to investigate the underlying mechanisms. AgNP-PEG-TC demonstrated stable colloidal properties and successful pH-sensitive release. It selectively reduced neurofibroma cell growth, migration, and invasion while promoting apoptosis, with minimal effects on normal cells. In xenograft models, AgNP-PEG-TC significantly inhibited tumor growth and showed good biocompatibility. Multi-omics analyses indicated that its antitumor activity was associated with ACSL4 downregulation, remodeling of arachidonic-acid-enriched phospholipids, enhanced lipid peroxidation, and increased lipid-droplet accumulation, suggesting heightened ferroptosis susceptibility. Notably, AgNP-PEG-TC synergized with MEK inhibitors and restored antitumor responses in resistant neurofibroma cells. These findings establish a metabolism-nanotechnology synergy in which AgNP-PEG-TC-mediated ACSL4 inhibition and lipid metabolic reprogramming resensitize MEK inhibitor-resistant neurofibromas to therapy. The platform functions as both a targeted drug carrier and a modulator of tumor lipid homeostasis, offering a promising combinatorial strategy.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><img></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":"2026-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004375","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":"Neutrophil extracellular traps in post-traumatic urethral microenvironment promote hypertrophic urethral stricture via the TLR9/NF-kB/Smad3/IL-8 axis","authors":"Ye-Hui Chen,&nbsp;Zhi-Bin Ke,&nbsp;Bo-Han Lin,&nbsp;Yi-Cheng Xu,&nbsp;Xue-Yi Xue,&nbsp;Qing-Shui Zheng,&nbsp;Xiong-Lin Sun,&nbsp;Yong Wei,&nbsp;Ying-Chun Liang,&nbsp;Ning Xu","doi":"10.1007/s10495-026-02368-1","DOIUrl":"10.1007/s10495-026-02368-1","url":null,"abstract":"<div><h3>Introduction</h3><p>Post-traumatic urethral stricture, characterized by hypertrophic scar formation, poses significant therapeutic challenges. Infiltration of neutrophil extracellular traps (NETs) is a prominent feature of post-traumatic urethral microenvironment, but their roles remain unknown.</p><h3>Objectives</h3><p>To investigate the mechanisms by which NETs mediate urethral fibrosis and explore potential therapeutic strategies targeting NETs.</p><h3>Methods</h3><p>Single-cell RNA sequencing was performed on urethral tissues from New Zealand rabbits with urethral injury to reveal the cell atlas of post-traumatic inflammatory microenvironment. The level of was assessed in both clinical and animal samples using immunohistochemistry and ELISA. In vitro, NETs were co-cultured with urethral fibroblasts (UFBs) to assess their effects and the mechanism underlying. Additionally, animal models of urethral injury were treated with NETs inhibitors to assess the effects of NETs on urethral scar formation.</p><h3>Results</h3><p>We constructed a single-cell atlas of the post-traumatic urethral microenvironment and found that NETs infiltration was correlated closely with the development of urethral fibrosis. NETs activated UFBs via the TLR9/NF-κB/Smad3 pathway, promoting collagen synthesis and IL-8 secretion, which further recruited neutrophils, creating a positive feedback loop. In vivo, DNase I and AT791 significantly reduced NET levels, suppressed fibroblast activation, and mitigated collagen deposition, effectively reducing stricture formation.</p><h3>Conclusion</h3><p>NETs drive post-traumatic urethral fibrosis by activating fibroblasts and amplifying inflammation. Targeting NETs or their uptake via TLR9 inhibition may offer a promising therapeutic strategy for urethral stricture.</p><h3>Graphical abstract</h3><p>NETs drive post-traumatic urethral fibrosis by activating fibroblasts and amplifying inflammation. Targeting NETs or their uptake via TLR9 inhibition may offer a promising therapeutic strategy for urethral stricture.</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":"2026-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148009356","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":"Disulfidptosis in hepatocellular carcinoma: molecular mechanisms, therapeutic potential, and exploratory insights into chronic liver diseases","authors":"Yuting Liu,&nbsp;Wenzhuo Hu,&nbsp;Jingyin Mai,&nbsp;Yang Cheng","doi":"10.1007/s10495-026-02363-6","DOIUrl":"10.1007/s10495-026-02363-6","url":null,"abstract":"<div><p>Disulfidptosis, a newly identified form of programmed cell death (PCD) that was discovered in 2023, occurs specifically in cells with high <i>SLC7A11</i> expression when glucose is scarce. The underlying mechanism involves NADPH depletion, which triggers severe disulfide stress and ultimately causes the actin cytoskeleton to collapse. In recent years, researchers have increasingly focused on the potential role of disulfidptosis in liver diseases. Current evidence mainly supports its involvement in hepatocellular carcinoma (HCC), with some preliminary data also suggesting connections to liver cirrhosis and metabolic liver disorders. This review critically synthesizes the molecular mechanisms underlying disulfidptosis, explores its possible links to various liver conditions based on the available evidence, and assesses the potential of disulfidptosis-related genes (<i>DRGs</i>) as exploratory tools for diagnosis, prognostic stratification, and exploratory therapeutic prediction. Together, these insights provide a foundation for understanding liver disease pathogenesis and may guide future research efforts, pending rigorous experimental and clinical validation.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004336","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":"Identifying Neddylation-modified features to assess prognosis and immune efficacy in hepatocellular carcinoma","authors":"Zitao Liu,&nbsp;Cheng Zuo,&nbsp;Changlei Wu,&nbsp;Huakai Tian,&nbsp;Zhengming Zhu,&nbsp;Wenjie Zhu,&nbsp;Liang Sun","doi":"10.1007/s10495-026-02339-6","DOIUrl":"10.1007/s10495-026-02339-6","url":null,"abstract":"<div><p>The Neddylation pathway is excessively activated in the occurrence and development of various cancers. However, there is currently a lack of comprehensive analysis of the Neddylation pathway in hepatocellular carcinoma (HCC). We treated HCC cells with a Neddylation pathway inhibitor (MLN4924) to observe its effects on the biological functions of HCC cells. Additionally, we constructed a Neddylation-related risk score (NRS) in HCC. Subsequently, we assessed the clinical value of NRS in predicting the prognosis of HCC and the efficacy of immunotherapy. Finally, we investigated the role of Proteasome 26S Subunit, Non-ATPase 1 (PSMD1) in the malignant progression of HCC through in vivo and in vitro experiments. MLN4924 significantly inhibits the proliferation and migratory capacity of HCC cells, promotes apoptosis, and upregulates PD-L1 expression. Moreover, we have confirmed through in vivo and in vitro experiments that MLN4924 can enhance the sensitivity to Sorafenib. Additionally, we found that patients in the high NRS group have poor prognoses and are prone to developing resistance to treatments such as Sorafenib and Oxaliplatin, while being more sensitive to 5-Fluorouracil and immunotherapy. Finally, in both in vitro and in vivo experiments, it was found that knocking down PSMD1 can weaken the proliferation and metastatic capacity of HCC cells. Furthermore, knocking down PSMD1 can inhibit the levels of PD-L1 protein and NEDD8 protein that binds to Cullin in HCC cells. Mechanistically, we found that PSMD1 stabilizes the protein expression of β-catenin by inhibiting its degradation through the ubiquitin–proteasome system, thereby influencing the expression of PD-L1. In conclusion, this study reveals that Neddylation-related characteristics can effectively predict the prognosis and immunotherapy outcomes of HCC. Furthermore, targeting PSMD1 may represent a potential therapeutic approach for HCC.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":"31 6","pages":""},"PeriodicalIF":8.1,"publicationDate":"2026-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148009357","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}