Cell Death & Disease最新文献

{"title":"Correction: Circ0515 reprogramming mitochondrial succinate metabolism and promotes lung adenocarcinoma progression through regulating SDHB.","authors":"Yixiao Yuan, Yue Wu, Chunhong Li, Zuotian Huang, Dadi Peng, Zhongjun Wu, Xiulin Jiang","doi":"10.1038/s41419-026-08999-1","DOIUrl":"10.1038/s41419-026-08999-1","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13396382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148577054","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":"Chidamide induces ROS-driven ZAKα-dependent ribotoxic stress in endometrial cancer and enhances radiosensitivity in vitro and in vivo.","authors":"Haocheng Zhang, Zhiling Wang, Xinqin He, Yulong Mu, Xiaonan Fan, Xuan Wei, Hongluan Mao, Shuqi Chi, Zunling Li, Xuehui Pang, Wei Lu, Beihua Kong, Qing Zhang, Yingxin Pang","doi":"10.1038/s41419-026-09125-x","DOIUrl":"https://doi.org/10.1038/s41419-026-09125-x","url":null,"abstract":"<p><p>Chidamide is a selective histone deacetylase inhibitor with antitumor activity in several malignancies, but its mechanism of action in endometrial cancer (EC) remains poorly understood. In this study, we investigated the cytotoxic effects and underlying mechanism of chidamide in EC using cell lines, patient-derived organoids (PDOs), cell-derived xenograft (CDX) models, and patient-derived xenograft (PDX) models. Chidamide markedly inhibited EC cell growth and induced reactive oxygen species (ROS) accumulation, DNA damage, G2/M-phase arrest, and apoptosis. Mechanistically, transcriptomic and functional analyses showed that chidamide disrupted translational homeostasis and activated a ROS-dependent, ZAKα-mediated ribotoxic stress response, leading to p38 and JNK activation. Scavenging ROS with N-acetylcysteine (NAC) attenuated ZAKα-MAPK signaling, and partially rescued chidamide-induced cell cycle arrest and apoptosis. Similarly, pharmacological ZAK inhibition or ZAKα silencing weakened stress signaling and diminished the cytotoxic effects of chidamide, supporting the central role of the ROS-ZAKα-MAPK axis. Chidamide also activated the GCN2-eIF2α-ATF4 integrated stress response, and ISRIB further enhanced stress signaling and apoptosis, suggesting an adaptive buffering role of this pathway. In addition to its activity in vitro, chidamide showed broad antitumor efficacy in PDO, CDX, and PDX models. Chidamide also enhanced tumor radiosensitivity in vivo, supporting its potential utility in combination with radiotherapy. Together, these findings identify ROS-driven, ZAKα-dependent ribotoxic stress signaling as a key mechanism underlying chidamide-induced cytotoxicity in EC and provide a mechanistic rationale for the further development of chidamide-based strategies in this disease.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLC25A20 promotes tumor growth by reprogramming energy metabolism in lung adenocarcinoma.","authors":"Xing Liu, Xiaoyu Song, Cong Gan, Ye Wang, Mingxin Ni, Min Zhang, Shaodi Wen, Yahui Cao, Changhua Yi, Man Tian, Apeng Chen","doi":"10.1038/s41419-026-09119-9","DOIUrl":"https://doi.org/10.1038/s41419-026-09119-9","url":null,"abstract":"<p><p>Accumulating evidence has shown that the dysfunction of mitochondria, the multifunctional organelles in various cellular processes, is a pivotal event in the development of various diseases, including human cancers. The molecular alterations in tumors that promote metabolic diversity and distinct targetable dependencies remain poorly defined. The mitochondrial transporter SLC25A20, also known as carnitine-acylcarnitine translocase (CACT), is crucial for fatty acid β-oxidation (FAO) by importing acylcarnitines into the mitochondrial matrix. Here, we demonstrate that SLC25A20 is significantly upregulated in lung adenocarcinoma (LUAD) tissues and cells, and its expression correlates with poor patient survival. Gain- and loss-of-function experiments reveal that SLC25A20 promotes tumor cell proliferation, survival, migration, and invasion by enhancing FAO-associated mitochondrial bioenergetics and suppressing apoptosis. Mechanistically, SLC25A20-mediated FAO maintains mitochondrial function and supports oxidative phosphorylation (OXPHOS), thereby sustaining tumor bioenergetics and redox homeostasis. Pharmacological inhibition or genetic silencing of SLC25A20 impairs tumor growth in vivo. These findings establish SLC25A20 as a key metabolic driver in LUAD and suggest it may be a therapeutic target.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IGFBP5 derived from endothelial cells drive vascular invasion and liver metastasis of colorectal cancer by activating the ITGB3/PI3K/AKT Axis.","authors":"Nuersimanguli Maimaitiming, Yiqiao Deng, Huayuan Liu, Junshuai Xue, Chengyao Guo, Xiaomeng Liu, Bingzhi Wang, Xiao Chen, Zhen Huang, Hong Zhao, Jianqiang Cai","doi":"10.1038/s41419-026-09081-6","DOIUrl":"https://doi.org/10.1038/s41419-026-09081-6","url":null,"abstract":"<p><p>Vascular invasion (VascI) is a critical step in colorectal cancer (CRC) metastasis, but how specific cells in the tumor microenvironment (TME) regulate this process remains unclear, particularly the role of endothelial cells (ECs). Here, we found that vascular invasion is strongly associated with distant metastasis and poor prognosis in CRC patients. Analysis of single-cell RNA sequencing (scRNA-seq) data from 8 colorectal cancer liver metastases (CRLMs), included 4 VascI⁺ CRLMs and 4 VascI^- CRLMs, and identified 10 distinct EC subpopulations. Notably, an IGFBP5_tipECs significantly enriched in VascI⁺ CRLMs. High IGFBP5 expression correlated with VascI⁺ status and poor patient prognosis. Functionally, IGFBP5 overexpression (OE) in human umbilical vein endothelial cells (HUVECs) enhanced EC migration, tube formation, barrier disruption, and endothelial-to-mesenchymal transition (EndMT). In co-culture system, IGFBP5-OE ECs promoted malignant epithelial cells (MCs) proliferation, migration, and adhesion, and accelerated the growth of patient-derived CRC organoids. Mechanistically, RNA sequencing nominated ITGB3 as a key downstream effector, with activation of the PI3K/AKT signaling pathway. We confirmed a direct ligand-receptor interaction between EC-derived IGFBP5 and ITGB3 on MCs using multiplex immunofluorescence (mIF), co-immunoprecipitation (Co-IP), and proximity ligation assays (PLA). This interaction activated PI3K/AKT signaling in MCs, driving aggressive behavior both in vitro and in vivo, an effect that was significantly attenuated by ITGB3 silencing in MCs. Our findings identify IGFBP5-OE ECs as a key driver of VascI and liver metastasis in CRC via the ITGB3/PI3K/AKT axis, highlighting a potential therapeutic target to suppress metastatic progression.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149223347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting SLC1A5-mediated glutamine metabolism overcomes PARP inhibitor resistance in ovarian cancer.","authors":"Fang Han, Hongjie Du, Kunlin Tian, Gonghua Qi, Beihua Kong, Xia Luo, Hanlin Ma","doi":"10.1038/s41419-026-09123-z","DOIUrl":"10.1038/s41419-026-09123-z","url":null,"abstract":"<p><p>Poly(ADP-ribose) polymerase inhibitors (PARPi), such as olaparib, have significantly improved outcomes in ovarian cancer (OC); however, therapy resistance remains a major clinical challenge. Here, we showed that glutamine metabolism was upregulated in PARPi-resistant OC cells and identified the glutamine transporter SLC1A5 as a key mediator of this metabolic adaptation. Inhibition of SLC1A5 increased the sensitivity of OC cells to olaparib both in vitro and in vivo. Mechanistically, we demonstrated that the deubiquitinating enzyme USP14 directly interacted with and stabilized SLC1A5 by removing K48-linked polyubiquitin chains, thereby enhancing glutamine uptake, promoting glutathione synthesis, alleviating oxidative stress, and activating the mTORC1 pathway. This metabolic rewiring improved DNA damage repair capacity and ultimately contributed to PARPi resistance. Notably, combined treatment with the SLC1A5 inhibitor V-9302 and olaparib synergistically suppressed tumor growth in a patient-derived xenograft (PDX) model. Collectively, our findings identify the USP14-SLC1A5 axis as a novel regulator of PARPi resistance and suggest that targeting glutamine metabolism represents a promising therapeutic strategy to overcome PARPi resistance in ovarian cancer.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149219753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Atp8a2 drives neurodegeneration through the dysregulation of spatiotemporal phosphatidylserine externalization in mature neurons.","authors":"Adriana Schneider, Alexandra B Merkel, Nunzio Perta, Lisa Ruff, Netta Ussyshkin, Paula Zimmer, Bahar Aksan, Amandine Lepeuve, Laura D'Andrea, Silvia Pelucchi, Elena Marcello, Daniele Di Marino, Daniela Mauceri","doi":"10.1038/s41419-026-09097-y","DOIUrl":"10.1038/s41419-026-09097-y","url":null,"abstract":"<p><p>Phosphatidylserine (PS) asymmetry in plasma membranes is critical for cellular functions and serves as an apoptotic signal in many cell types. However, in mature neurons, the molecular mechanisms governing PS distribution, its precise regulation, and its functional significance beyond apoptosis and development remain poorly understood - particularly in the context of neurodegeneration. Here, we mapped the spatiotemporal dynamics of PS exposure in mature hippocampal neurons under physiological and pathological conditions using time-lapse imaging, revealing specific PS externalization hotspots at dendritic branching points. Using multiple in vitro and in vivo neurodegeneration models combined with molecular modeling, RNA interference, pharmacological interventions, and biochemical assays, we identified Atp8a2 as the primary regulator of PS asymmetry in mature neurons beyond its known roles in development. Notably, Atp8a2 expression levels - rather than its flippase activity alone - were essential for maintaining neuronal structural integrity and viability. Atp8a2 expression was significantly altered by neurotoxic stimuli and in multiple mouse models of neurodegeneration. Reduced Atp8a2 expression led to increased PS exposure, compromised neuronal architecture, and heightened susceptibility to degeneration, whereas Atp8a2 overexpression conferred substantial neuroprotection. The distinction between Atp8a2's enzymatic activity and expression level reveals a mechanism of neuronal homeostasis linking PS regulation to structural integrity and survival, possibly through association with cytoskeletal protein networks. Thus, Atp8a2 expression is a critical determinant of mature neuronal viability, presenting a potential target for neuroprotective strategies in neurodegeneration.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13392023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148560994","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":"AARS1-catalyzed H4K12 lactylation promotes HCC resistance to targeted therapy by activating RAPGEF3-RAP1 signaling.","authors":"Tanlun Zeng, Wanwan Zhu, Guanqun Sun, Tengjiao Wang, Chenna Liu, Guanghui Hu, Junyu Liu, Pengyun Ling, Li Wang, Chang Fan, Terence Kin Wah Lee, Jianru Xiao, Xijun Liang, Jin Ding","doi":"10.1038/s41419-026-09011-6","DOIUrl":"10.1038/s41419-026-09011-6","url":null,"abstract":"<p><p>Although receptor tyrosine kinase inhibitors (sorafenib and lenvatinib) have been applied as a first-line targeted therapy for advanced unresectable hepatocellular carcinoma (HCC) for decades, their clinical efficacy is limited and the underlying mechanism remains unclear. HCC is a highly glycolytic malignancy characterized by excessive lactate accumulation in the tumor microenvironment (TME). Emerging evidences show that histone lactylation plays a critical role in various biological processes, but its function in receptor tyrosine kinase inhibitor resistance remains obscure. This study was designed to elucidate the role of histone lactylation in receptor tyrosine kinase inhibitor resistance in HCC. Clinical cohort analyses revealed that the increased nuclear pan-lysine lactylation (pan-Kla) predicts poor patient prognosis and high H4K12la level correlates with targeted drug resistance. Furthermore, lactate bidirectionally controls H4K12la through the opposing enzymatic activities of AARS1 (writer) and HDAC11 (eraser). Integrative CUT&Tag and ATAC-seq analyses demonstrated that H4K12la directly activates the promoter of RAPGEF3, a predominant upstream regulator of the RAP1 signaling pathway. Inhibition of RAPGEF3 reversed the lactate-induced targeted drug resistance both in vitro and in vivo, suggesting H4K12 lactylation modulates targeted drug resistance by activating RAPGEF3-RAP1 signaling. Notably, combining the RAPGEF3 inhibitor ESI-09 with lenvatinib synergistically suppressed HCC growth in mouse models. Clinico-pathological analyses revealed that elevated expression of the AARS1/H4K12la/RAPGEF3 axis correlated with inferior survival and sorafenib resistance in HCC patients, which was further confirmed in patient-derived xenograft (PDX) models. This study delineates a novel metabolic-epigenetic mechanism whereby lactate modulates hepatocellular carcinoma sensitivity to targeted therapies through histone lactylation and suggests AARS1-H4K12la-RAPGEF3 axis may serve as an interventional target to overcome targeted drug resistance, offering a promising strategy to enhance clinical outcomes in HCC patients.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148547920","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":"Rewiring cell death, metabolism and immunity in precision medicine: insights from the CDDisease 12th Meeting.","authors":"Peishan Li, Mauro Piacentini, Yufang Shi, Gerry Melino","doi":"10.1038/s41419-026-09017-0","DOIUrl":"10.1038/s41419-026-09017-0","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148547908","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":"LSD1-GLS2 axis drives subtype-specific chemoresistance in pancreatic cancer through glutaminolysis reprogramming.","authors":"Zhefang Wang, Qiu Huang, Jiangang Zhao, Zicheng Lyu, Feng Ju, Bo You, Jie Wang, Qiongzhu Dong, Margarete Odenthal, Alexander Quaas, Kalliope N Diakopoulos, Hana Algül, Maximilian Reichert, Christiane J Bruns, Yue Zhao","doi":"10.1038/s41419-026-09075-4","DOIUrl":"10.1038/s41419-026-09075-4","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) remains a highly lethal malignancy due to its aggressive biology and therapeutic resistance. Lysine-specific demethylase 1 (LSD1), an epigenetic regulator, is overexpressed in PDAC and linked to poor prognosis, yet its context-dependent roles in metabolic subtypes and chemoresistance remain undefined. Here, we show that LSD1 knockdown has opposing, subtype-specific effects on chemotherapeutic responses: it sensitized RSK-subtype cells (L3.6pl, PANC-1) to chemotherapy but induced resistance in KRAS-subtype cells (BxPC-3, TBO368). Integrated analyses revealed mitochondrial dysfunction and defective mitophagy as hallmarks distinguishing KRAS- from RSK-subtype PDAC. Critically, mitochondrial targeting through respiratory modulation or mitophagy manipulation overrides LSD1-mediated subtype-specific chemoresistance, establishing mitochondrial fitness as the mechanistic determinant. Mechanistically, LSD1 transcriptionally regulates GLS2 to drive glutamine metabolic reprogramming, promoting reductive carboxylation in KRAS-subtype cells and oxidative metabolism in RSK-subtype cells. Our work establishes the LSD1-GLS2 axis as a metabolic switch controlling PDAC chemosensitivity and provides a framework for subtype-specific therapeutic strategies.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":"17 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13385623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535421","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":"Tubular tRF‑1:30‑Gln‑CTG‑4 attenuates tubulointerstitial fibrosis by mitigating FBXO7-mediated mitophagy defect in diabetic kidney disease.","authors":"Jia-Ling Ji, Yun-Yang Qiao, Jia-Yue Sun, Ying Huo, Hui-Min Shi, Gao-Ting Qu, Shan-Wen Li, Chan Huang, Yu Feng, Pei Zhang, Ling Ding, Zuo-Lin Li, Ai-Qing Zhang","doi":"10.1038/s41419-026-09112-2","DOIUrl":"10.1038/s41419-026-09112-2","url":null,"abstract":"<p><p>Tubulointerstitial fibrosis (TIF) is a crucial pathological feature and inevitable consequence of progressive diabetic kidney disease (DKD). Transfer RNA-derived fragments (tRFs), a novel class of small non-coding RNA by cleavage of tRNAs, have recently attracted attention due to their functional significance in diverse biological processes. However, the role of tRFs in TIF is largely elusive. In the present study, we found that a tRF, tRF‑1:30‑Gln‑CTG‑4, was markedly decreased in proximal renal tubules and highly correlated with TIF in DKD mice. The overexpression of tRF‑1:30‑Gln‑CTG‑4 revealed a therapeutic effect against TIF. Further, RNA pull-down and RNA-immunoprecipitation assay were performed to identify that FBXO7, an adaptor protein in the SCF E3 ligase complex, was the targeted protein of tRF‑1:30‑Gln‑CTG‑4. Mass spectrometry and co-immunoprecipitation experiments revealed that PINK1, a master mitophagy-regulating protein, acted as the substrate of FBXO7 in tubular epithelial cells. Mechanistically, elevated FBXO7 promoted mitophagy defect through mediating PINK1 ubiquitylation and proteasomal degradation. The overexpression of tRF‑1:30‑Gln‑CTG‑4 alleviated defective mitophagy. Taken together, this study not only represents a novel insight into the pathogenesis of TIF but also provides a promising therapeutic targeting for the delaying the progression of DKD.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":" ","pages":""},"PeriodicalIF":12.2,"publicationDate":"2026-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148497219","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}