Cell Death & Disease最新文献

{"title":"Human proximal tubular epithelial cell interleukin-1 receptor signalling triggers G2/M arrest and cellular senescence during hypoxic kidney injury.","authors":"Kurt T K Giuliani, Purba Nag, Benjamin C Adams, Xiangju Wang, Seokchan Hong, Anca Grivei, Rebecca L Johnston, Nicola Waddell, Kenneth K C Ho, Yilin Tian, Muhammad Ali Khan, Chang Seong Kim, Monica S Y Ng, Glenda Gobe, Jacobus P J Ungerer, Josephine M Forbes, Helen G Healy, Andrew J Kassianos","doi":"10.1038/s41419-025-07386-6","DOIUrl":"10.1038/s41419-025-07386-6","url":null,"abstract":"<p><p>Hypoxia and interleukin (IL)-1β are independent mediators of tubulointerstitial fibrosis, the histological hallmark of chronic kidney disease (CKD). Here, we examine how hypoxia and IL-1β act in synergy to augment maladaptive proximal tubular epithelial cell (PTEC) repair in human CKD. Ex vivo patient-derived PTECs were cultured under normoxic (21% O₂) or hypoxic (1% O₂) conditions in the absence or presence of IL-1β and examined for maladaptive repair signatures. Hypoxic PTECs incubated with IL-1β displayed a discrete transcriptomic profile distinct from PTECs cultured under hypoxia alone, IL-1β alone or under normoxia. Hypoxia+IL-1β-treated PTECs had 692 'unique' differentially expressed genes (DEGs) compared to normoxic PTECs, with 'cell cycle' the most significantly enriched KEGG pathway based on 'unique' down-regulated DEGs (including CCNA2, CCNB1 and CCNB2). Hypoxia+IL-1β-treated PTECs displayed signatures of cellular senescence, with reduced proliferation, G2/M cell cycle arrest, increased p21 expression, elevated senescence-associated β-galactosidase (SA-β-gal) activity and increased production of pro-inflammatory/fibrotic senescence-associated secretory phenotype (SASP) factors compared to normoxic conditions. Treatment of Hypoxia+IL-1β-treated PTECs with either a type I IL-1 receptor (IL-1RI) neutralizing antibody or a senolytic drug combination, quercetin+dasatinib, attenuated senescent cell burden. In vitro findings were validated in human CKD bio-specimens (kidney tissue, urine), with elevated PTEC IL-1RI expression and senescence (SA-β-gal activity) detected in fibrotic kidneys and numbers of senescent (SA-β-gal⁺) urinary PTECs correlating with urinary IL-1β levels and severity of interstitial fibrosis. Our data identify a mechanism whereby hypoxia in combination with IL-1β/IL-1RI signalling trigger PTEC senescence, providing novel therapeutic and diagnostic check-points for restoring tubular regeneration in human CKD.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"61"},"PeriodicalIF":8.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785723/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074008","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}

{"title":"Estrogen-dependent activation of TRX2 reverses oxidative stress and metabolic dysfunction associated with steatotic disease.","authors":"Alfredo Smiriglia, Nicla Lorito, Marina Bacci, Angela Subbiani, Francesca Bonechi, Giuseppina Comito, Marta Anna Kowalik, Andrea Perra, Andrea Morandi","doi":"10.1038/s41419-025-07331-7","DOIUrl":"10.1038/s41419-025-07331-7","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum of hepatic disorders, ranging from simple steatosis to steatohepatitis, with the most severe outcomes including cirrhosis, liver failure, and hepatocellular carcinoma. Notably, MASLD prevalence is lower in premenopausal women than in men, suggesting a potential protective role of estrogens in mitigating disease onset and progression. In this study, we utilized preclinical in vitro models-immortalized cell lines and hepatocyte-like cells derived from human embryonic stem cells-exposed to clinically relevant steatotic-inducing agents. These exposures led to lipid droplet (LD) accumulation, increased reactive oxygen species (ROS) levels, and mitochondrial dysfunction, along with decreased expression of markers associated with hepatocyte functionality and differentiation. Estrogen treatment in steatotic-induced liver cells resulted in reduced ROS levels and LD content while preserving mitochondrial integrity, mediated by the upregulation of mitochondrial thioredoxin 2 (TRX2), an antioxidant system regulated by the estrogen receptor. Furthermore, disruption of TRX2, either pharmacologically using auranofin or through genetic interference, was sufficient to counteract the protective effects of estrogens, highlighting a potential mechanism through which estrogens may prevent or slow MASLD progression.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"57"},"PeriodicalIF":8.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074002","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}

{"title":"Smad4 deficiency in hepatocytes attenuates NAFLD progression via inhibition of lipogenesis and macrophage polarization.","authors":"Wei Yang, Xuanxuan Yan, Rui Chen, Xin Xin, Shuang Ge, Yongxiang Zhao, Xinlong Yan, Jinhua Zhang","doi":"10.1038/s41419-025-07376-8","DOIUrl":"10.1038/s41419-025-07376-8","url":null,"abstract":"<p><p>Nonalcoholic fatty liver disease (NAFLD), a major cause of chronic liver disorders, has become a serious public health issue. Although the Smad4 signaling pathway has been implicated in the progression of NAFLD, the specific role of Smad4 in hepatocytes in NAFLD pathogenesis remains unclear. Hepatocyte-specific knockout Smad4 mice (Alb^Smad4-/-) were first constructed using the Cre-Loxp recombinant system to establish a high-fat diet induced NAFLD model. The role of Smad4 in the occurrence and development of NAFLD was determined by monitoring the body weight of mice, detecting triglycerides and free fatty acids in serum and liver tissue homogenates, staining the tissue sections to observe the accumulation of liver fat, and RT-qPCR detecting the expression of genes related to lipogenesis, fatty acid intake, and fatty acid β oxidation. The molecular mechanism of Smad4 in hepatocytes affecting NAFLD was therefore investigated through combining in vitro and in vivo experiments. Smad4 deficiency in hepatocytes mitigated NAFLD progression and decreased inflammatory cell infiltration. Moreover, Smad4 deficiency inhibited CXCL1 secretion by suppressing the activation of the ASK1/P38/JNK signaling pathway. Furthermore, targeting CXCL1 using CXCR2 inhibitors diminished hepatocyte lipogenesis and inhibited the polarization of M1-type macrophages. Collectively, these results suggested that Smad4 plays a vital role in exacerbating NAFLD and may be a promising candidate for anti-NAFLD therapy.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"58"},"PeriodicalIF":8.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074017","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}

{"title":"Histone lactylation promotes multidrug resistance in hepatocellular carcinoma by forming a positive feedback loop with PTEN.","authors":"Yuan Zeng, Haoran Jiang, Zhoufeng Chen, Jun Xu, Xiangting Zhang, Weimin Cai, Xianjie Zeng, Peipei Ma, Rong Lin, Huilin Yu, Yuanhang He, Huiya Ying, Ruoru Zhou, Xiao Wu, Fujun Yu","doi":"10.1038/s41419-025-07359-9","DOIUrl":"10.1038/s41419-025-07359-9","url":null,"abstract":"<p><p>FOLFOX (5-fluorouracil, oxaliplatin, folinic acid) is a standard treatment for hepatocellular carcinoma, but its efficacy is often limited by drug resistance, the underlying mechanisms of which remain unclear. In this study, oxaliplatin (OXA)- and 5-fluorouracil (5-Fu)-resistant hepatocellular carcinoma cell lines were established, and enhanced glycolytic activity was identified in resistant cells. Inhibiting glycolysis effectively suppressed the malignant behavior of both OXA- and 5-Fu-resistant cells. Mechanistically, active glycolysis induced elevated levels of lactylation, predominantly histone lactylation, with H3K14la playing a key role in regulating gene expression. The ubiquitin E3 ligase NEDD4 was identified as a downstream target of H3K14la. Furthermore, NEDD4, regulated by histone lactylation, interacted with PTEN to mediate its ubiquitination and subsequent degradation. The downregulation of PTEN formed a positive feedback loop, further driving the malignant progression of OXA- and 5-Fu-resistant cells. This study elucidates a shared mechanism underlying OXA and 5-Fu resistance in hepatocellular carcinoma and highlights a promising therapeutic target for overcoming clinical chemotherapy resistance.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"59"},"PeriodicalIF":8.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074005","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}

{"title":"Piezo1-directed neutrophil extracellular traps regulate macrophage differentiation during influenza virus infection.","authors":"Yuexin Wang, Qiuli Yang, Yingjie Dong, Likun Wang, Zhiyuan Zhang, Ruiying Niu, Yufei Wang, Yujing Bi, Guangwei Liu","doi":"10.1038/s41419-025-07395-5","DOIUrl":"10.1038/s41419-025-07395-5","url":null,"abstract":"<p><p>Neutrophils and macrophages are critical for antiviral immunity, but their reciprocal regulatory roles and mechanisms in the response to viral infection remain unclear. Herein, we found that the ion channel Piezo1 directs neutrophil extracellular trap (NET) formation and regulates macrophage functional differentiation in anti-influenza virus immunity. Genetic deletion of Piezo1 in neutrophils inhibited the generation of NETs and M1 macrophage differentiation while driving the development of M2 macrophages during viral infection. Piezo1-directed neutrophil NET DNA directly regulates macrophage differentiation in vitro and in vivo. Mechanistically, neutrophil Piezo1 deficiency inhibited NET DNA production, leading to decreased TLR9 and cGAS-STING signalling activity while inducing reciprocal differentiation from M1 to M2 macrophages. In addition, Piezo1 integrates magnesium signalling and the SIRT2-hypoxia-inducible factor-1 alpha (HIF1α)-dependent pathway to orchestrate reciprocal M1 and M2 macrophage lineage commitment through neutrophil-derived NET DNA. Our studies provide critical insight into the role of neutrophil-based mechanical regulation of immunopathology in directing macrophage lineage commitment during the response to influenza virus infection.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"60"},"PeriodicalIF":8.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11785962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143074014","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}

{"title":"Executioner caspases degrade essential mediators of pathogen-host interactions to inhibit growth of intracellular Listeria monocytogenes.","authors":"Marilyne Lavergne, Raffael Schaerer, Sara De Grandis, Safaa Bouheraoua, Oluwadamilola Adenuga, Tanja Muralt, Tiffany Schaerer, Léa Chèvre, Alessandro Failla, Patricia Matthey, Michael Stumpe, Dieter Kressler, Pierre-Yves Mantel, Michael Walch","doi":"10.1038/s41419-025-07365-x","DOIUrl":"10.1038/s41419-025-07365-x","url":null,"abstract":"<p><p>Cell death mediated by executioner caspases is essential during organ development and for organismal homeostasis. The mechanistic role of activated executioner caspases in antibacterial defense during infections with intracellular bacteria, such as Listeria monocytogenes, remains elusive. Cell death upon intracellular bacterial infections is considered altruistic to deprive the pathogens of their protective niche. To establish infections in a human host, Listeria monocytogenes deploy virulence mediators, including membranolytic listeriolysin O (LLO) and the invasion associated protein p60 (Iap), allowing phagosomal escape, intracellular replication and cell-to-cell spread. Here, by means of chemical and genetical modifications, we show that the executioner caspases-3 and -7 efficiently inhibit growth of intracellular Listeria monocytogenes in host cells. Comprehensive proteomics revealed multiple caspase-3 substrates in the Listeria secretome, including LLO, Iap and various other proteins crucially involved in pathogen-host interactions. Listeria secreting caspase-uncleavable LLO or Iap gained significant growth advantage in epithelial cells. With that, we uncovered an underappreciated defense barrier and a non-canonical role of executioner caspases to degrade virulence mediators, thus impairing intracellular Listeria growth.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"55"},"PeriodicalIF":8.1,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11782612/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063906","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}

{"title":"SP-1-activated LINC01016 overexpression promotes gastric cancer invasion and metastasis through inhibiting EIF4A3-mediated MMP9 mRNA decay.","authors":"Ying Sun, Hui Zhang, Duan-Bo Shi, Peng Gao","doi":"10.1038/s41419-024-07250-z","DOIUrl":"10.1038/s41419-024-07250-z","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) are key regulators during gastric cancer (GC) development and may be viable treatment targets. In the present study, we showed that the expression of the long intergenic noncoding RNA 01016 (LINC01016) is significantly higher in GC tissues with lymph node metastasis (LNM) than those without LNM. LINC01016 overexpression predicts a poorer relapse-free survival (RFS) and overall survival (OS). Furthermore, we found that LINC01016 is activated by transcriptional factor SP-1 and contributes to the overt promotion of cell migratory ability. EIF4A3 was identified as a binding partner of LINC01016 by RNA pull-down assay, mass spectrometry and western blot. We determined that LINC01016 can blocks the binding of EIF4A3 to MMP9 mRNA, thereby inhibiting EIF4A3-mediated nonsense-mediated RNA decay (NMD), increasing MMP9 mRNA level and protein expression levels to promote tumor progression. LINC01016 or LINC01016-mediated EIF4A3/MMP9 may be potential therapeutic targets for patients with GC.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"54"},"PeriodicalIF":8.1,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11828860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063954","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}

{"title":"Skull bone marrow and skull meninges channels: redefining the landscape of central nervous system immune surveillance.","authors":"Liang Liu, Xian Zhang, Yan Chai, Jianning Zhang, Quanjun Deng, Xin Chen","doi":"10.1038/s41419-025-07336-2","DOIUrl":"10.1038/s41419-025-07336-2","url":null,"abstract":"<p><p>The understanding of neuroimmune function has evolved from concepts of immune privilege and protection to a new stage of immune interaction. The discovery of skull meninges channels (SMCs) has opened new avenues for understanding central nervous system (CNS) immunity. Here, we characterize skull bone marrow and SMCs by detailing the anatomical structures adjacent to the skull, the differences between skull and peripheral bone marrow, mainstream animal processing methods, and the role of skull bone marrow in monitoring various CNS diseases. Additionally, we highlight several unresolved issues based on current research findings, aiming to guide future research directions.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"53"},"PeriodicalIF":8.1,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058091","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}

{"title":"Targeting glycolytic reprogramming by tsRNA-0032 for treating pathological lymphangiogenesis.","authors":"Fan Ye, Ziran Zhang, Lianjun Shi, Shuting Lu, Xiumiao Li, Wan Mu, Qin Jiang, Biao Yan","doi":"10.1038/s41419-025-07366-w","DOIUrl":"10.1038/s41419-025-07366-w","url":null,"abstract":"<p><p>Lymphangiogenesis is vital for tissue fluid homeostasis, immune function, and lipid absorption. Abnormal lymphangiogenesis has been implicated in several diseases such as cancers, inflammatory, and autoimmune diseases. In this study, we elucidate the role of tsRNA-0032 in lymphangiogenesis and its molecular mechanism. tsRNA-0032 expression is significantly decreased in corneal suture model and human lymphatic endothelial cell (HLEC) model under inflammatory condition. Overexpression of tsRNA-0032 exerts anti-lymphangiogenic effects by inhibiting HLEC proliferation, migration, and tube formation. Moreover, overexpression of tsRNA-0032 inhibits suture-induced corneal lymphangiogenesis. tsRNA-0032 is mainly located in the cytoplasm and interacts with Ago2 protein. Overexpression of tsRNA-0032 reduces ATP production and decreases pyruvate and lactate levels by targeting PKM2, a key enzyme in glycolysis. This regulation of glycolysis alters cellular energy and metabolic balance in HLECs, contributing to anti-lymphangiogenic effects. Clinical data reveals that tsRNA-0032 levels are significantly reduced in corneal tissues of transplant recipients compared to donors, while PKM2 expression is elevated, highlighting the clinical relevance of tsRNA-0032/PKM2 axis in corneal lymphangiogenesis. This study offers new insights into the regulation of lymphangiogenesis and presents potential therapeutic targets for lymphangiogenesis-related diseases.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"51"},"PeriodicalIF":8.1,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11772812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051817","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}

{"title":"The E3-ligase Siah2 activates mitochondrial quality control in neurons to maintain energy metabolism during ischemic brain tolerance.","authors":"Maria Josè Sisalli, Elena D'Apolito, Ornella Cuomo, Giovanna Lombardi, Michele Tufano, Lucio Annunziato, Antonella Scorziello","doi":"10.1038/s41419-025-07339-z","DOIUrl":"10.1038/s41419-025-07339-z","url":null,"abstract":"<p><p>Mitochondrial quality control is crucial for the homeostasis of the mitochondrial network. The balance between mitophagy and biogenesis is needed to reduce cerebral ischemia-induced cell death. Ischemic preconditioning (IPC) represents an adaptation mechanism of CNS that increases tolerance to lethal cerebral ischemia. It has been demonstrated that hypoxia-induced Seven in absentia Homolog 2 (Siah2) E3-ligase activation influences mitochondrial dynamics promoting the degradation of mitochondrial proteins. Therefore, in the present study, we investigated the role of Siah2 in the IPC-induced neuroprotection in in vitro and in vivo models of IPC. To this aim, cortical neurons were exposed to 30-min oxygen and glucose deprivation (OGD, sublethal insult) followed by 3 h OGD plus reoxygenation (lethal insult). Our results revealed that the mitochondrial depolarization induced by hypoxia activates Siah2 at the mitochondrial level and increases LC3-II protein expression, a marker of mitophagy, an effect counteracted by the reoxygenation phase. By contrast, hypoxia reduced the expression of peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), a marker of mitochondrial biogenesis, whereas its expression was increased after reoxygenation thus improving mitochondrial membrane potential, mitochondrial calcium content, and mitochondrial morphology, hence leading to neuroprotection in IPC. Furthermore, Siah2 silencing confirmed these results. Collectively, these findings indicate that the balance between mitophagy and mitochondrial biogenesis, due to the activation of the Siah2-E3-ligase, might play a role in IPC-induced neuroprotection.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"16 1","pages":"52"},"PeriodicalIF":8.1,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058009","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}