Cell Death Discovery最新文献

{"title":"Enhanced precision in cell culture analytics: leveraging artificial intelligence for unbiased and non-destructive assessment of cell growth and viability.","authors":"Cheung Pang Wong, Nasrin Khazamipour, Soroush Aalibagi, Sukrit Kapoor, Louise Ramos, Joya Maria Saade, Casper Dolleris, Janny Marie L Peterslund, Daria Golnarian, Negin Farivar, Mads Daugaard, Nader Al Nakouzi","doi":"10.1038/s41420-026-03116-9","DOIUrl":"https://doi.org/10.1038/s41420-026-03116-9","url":null,"abstract":"<p><p>Precise assessment of cell growth, count, and viability is a prerequisite for biological and medical research. Traditional cell analytics involve manual processes, such as cell counting or reagent-based approaches that are user-dependent and prone to bias. Semi-automated systems for counting cells, tracking cell growth, and determining viability have been introduced over the past decades. However, these methods are often time-consuming, require labeling steps, and involve costly instrumentation and consumables. Changes in cell growth and/or viability create biological patterns that can be interpreted by artificial intelligence (AI). Here, we report the development and validation of SnapCyte™, an AI application that performs accurate, unbiased, label- and reagent-free cell analyses from basic cell culture images. Using cell lines with diverse morphologies in various culture conditions, we generated a comprehensive and fully annotated image database that was used for AI education. Convolutional neural networks were employed for cell localization and iterative training loops until a stable performance of >95% accuracy was obtained for all readouts. The fully trained AI demonstrated high Precision and Recall and performed with greater accuracy and less variation as compared to standard methods. As the SnapCyte analyses are performed on cell images only, data acquisition is non-invasive to the experimental setup, enabling real-time use of cells in downstream assays. In summary, SnapCyte is a fast and accurate cell analytics platform, resistant to user variations and independent of reagents or specific equipment, with improved performance over current cell analytics methodologies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670772","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 comparative analysis of serum and tissue proteomic profiles in non-small cell lung cancer patients with or without brain metastasis.","authors":"Yongtao Zheng, Yueting Xiong, Yuxiao Ma, Yijie Qiu, Qingfang Bu, Zhenxi Wang, Qingfang Sun, Yuhao Sun, Xiaohui Liu, Quan Yuan, Yuping Li, Liuguan Bian, Baofeng Wang","doi":"10.1038/s41420-026-03109-8","DOIUrl":"https://doi.org/10.1038/s41420-026-03109-8","url":null,"abstract":"<p><p>To identify specific, sensitive, and non-invasive circulating protein biomarkers that could facilitate the diagnosis of brain metastasis (BrM) and improve risk prediction for BrM among patients with non-small cell lung cancer (NSCLC). We performed data-independent acquisition mass spectrometry (DIA-MS)-based proteomic profiling of 14 tissue specimens obtained from 7 patients, together with 89 serum samples from NSCLC and NSCLC-BrM cohorts, to identify candidate biomarkers associated with BrM. A total of 12,808 proteins were identified in the tissue proteome and 6041 proteins in the serum proteome, representing an extensive proteomic analysis of lung cancer with BrM reported to date. Using integrated analyses, we identified a four-protein classifier that served as biomarkers for predicting the risk of NSCLC metastasis to the brain. Notably, PSMA4, LAP3, and LZIC were consistently downregulated in both the sera and tissues of patients with NSCLC-BrM compared with those with NSCLC without BrM. These biomarkers were subsequently validated by ELISA in an additional cohort, demonstrating high concordance with the PRM results. Immunohistochemical analyses further supported the utility of these proteins in distinguishing BrM from primary brain tumors. The integrated analysis of tissue and serum proteomics across the cohorts supports the potential value of proteomics-guided, biomarker-assisted diagnosis and risk prediction in BrM and may help enable more accurate stratification and more targeted treatment strategies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147670805","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":"High-throughput strategy for targeting MDM2 in uveal melanoma to reverse radiation therapy resistance.","authors":"Qi Zhu, Xi Gong, Sirong Zhang, Jiaqi Zhang, Hongtao Yan","doi":"10.1038/s41420-026-02970-x","DOIUrl":"https://doi.org/10.1038/s41420-026-02970-x","url":null,"abstract":"<p><p>Uveal melanoma (UM) presents a formidable clinical challenge due to its marked resistance to radiotherapy. In this study, an integrative strategy combining machine learning models with high-throughput screening platforms was employed to identify novel small-molecule inhibitors targeting MDM2, with the aim of overcoming this intrinsic resistance. Transcriptome sequencing and machine learning analysis identified MDM2 as a critical gene associated with UM radiotherapy resistance. Integration of single-cell RNA sequencing data revealed key cells contributing to this resistance. In vitro experiments demonstrated that the MDM2 inhibitor SAR405838 effectively increased radiosensitivity in resistant UM cells by modulating p53 activation, suppressing cell migration and invasion, and inducing DNA damage and apoptosis. This novel approach offers a promising therapeutic strategy for combating UM resistance to radiation therapy.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662260","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":"TREM2-mediated microglial phagocytosis of inhibitory synapses contributes to prolonged FS-induced epileptogenesis.","authors":"Xiaoqian Wang, Hua Zhou, Yujie Zhai, Yunrong Zhang, Yao Cheng, Yi Yuan, Wenxiao Cao, Anqing Gao, Mengshuang Liu, Qiaoyun Wang, Hongliu Sun","doi":"10.1038/s41420-026-03118-7","DOIUrl":"https://doi.org/10.1038/s41420-026-03118-7","url":null,"abstract":"<p><p>Febrile seizures (FS) are common convulsive episodes in childhood and an important etiological component in epilepsy. However, most currently available antiepileptic drugs cannot prevent epileptogenesis and may even exacerbate it. Triggering receptor expressed on myeloid cell 2 (TREM2)-mediated microglial phagocytosis of inhibitory synapses may play a pivotal role in epileptogenesis; however, the role of TREM2 in FS-induced epilepsy remains unclear. We established a Sprague-Dawley rat model of juvenile prolonged FS to analyze the associated molecular changes, epileptic susceptibility, and seizures. Our results confirmed that prolonged FS resulted in increased TREM2 levels, excessive phagocytosis by activated microglia targeting inhibitory synapses, and elevated epileptic susceptibility and seizures. Administration of a CD33 agonist (monosialoganglioside 1, GM1), a negative moderator of TREM2 that reduces its levels, attenuated microglial phagocytosis of inhibitory synapses and weakened susceptibility to epilepsy and seizures. The inhibitory effects of TREM2 knockdown were similar to those of CD33 activation. Blocking the outward-facing region of phosphatidylserine (PtdSer) to prevent TREM2 recognition resulted in increased TREM2 levels and deteriorated microglial activation. Finally, although vesicular GABA transporter (VGAT) levels were higher in the prolonged FS rats treated with annexin V, susceptibility to epilepsy and seizures were aggravated. This study revealed that reducing TREM2 levels may inhibit prolonged FS-induced epileptogenesis by alleviating the phagocytic function of activated microglia targeting inhibitory synapses, while preventing TREM2 from recognizing PtdSer has the opposite effect.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662272","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":"Bacterial protein-oleate complexes induce ferroptosis-like cell death in colorectal cancer cells by disrupting cell membranes and inhibiting the β-catenin-GPX4 axis.","authors":"Naeem Ullah, Abdelbasset Yabrag, Amjad Ali, Aftab Nadeem","doi":"10.1038/s41420-026-03097-9","DOIUrl":"10.1038/s41420-026-03097-9","url":null,"abstract":"<p><p>The tumoricidal activity of human α-lactalbumin complexes, such as HAMLET and its α-helical domain with sodium oleate, is well-documented. However, the potential of bacterial α-helical proteins to form analogous anticancer complexes remains unexplored. In the current study, we demonstrate that α-helical proteins of bacterial origin can form tumoricidal complexes with sodium oleate. Using non-hemolytic toxin A (NheA), an inactive component of the native tripartite (NheABC) toxin complex from Bacillus thuringiensis, we show that NheA, upon mixing with sodium oleate (NheA-O), forms potent tumoricidal complexes against colorectal cancer cells. The NheA-O complex binds to the plasma membrane of tumor cells, disrupting the function of cellular organelles and ultimately causing cell death. Mechanistically, NheA-O induces ACSL4 and suppresses GPX4 expression, which ultimately leads to the accumulation of lipid peroxidation, following suppression of β-catenin signaling. The suppression of β-catenin signaling and its target proteins ultimately leads to suppression of colorectal cancer tumorigenesis. Functionally, NheA-O inhibits tumor cell migration, spheroid formation, clonogenic potential, ATP production and induces lipid peroxidation. These findings establish that bacterial α-helical proteins, like their human counterparts, can be engineered to form tumoricidal complexes with sodium oleate. Our work highlights NheA-O as a novel candidate that causes activation of ferroptosis-like cell death in target cancer cells, leading to intracellular organelles dysfunction. Moreover, NheA-O activity synergizes with RSL3, and NheA-O mediated cell death is antagonized by Fer-1, indicating the role of NheA-O in inducing ferroptosis-like cell death. Overall, these results describe NheA-O as a novel therapeutic agent to combat tumorigenesis by targeting tumor cell membrane and proteasomal degradation of GPX4 to trigger ferroptosis-like cell death and expands the paradigm of tumoricidal protein-lipid complexes functionality across biological kingdoms.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13076691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662282","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":"Necrosis by sodium overload: a potential mechanism for renal diseases associated with mitochondrial dysfunction.","authors":"Quanhai Liu, Jiawei Lai, Jiancang Ma, Fangshi Xu","doi":"10.1038/s41420-026-03111-0","DOIUrl":"https://doi.org/10.1038/s41420-026-03111-0","url":null,"abstract":"","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653869","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":"Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).","authors":"Zhi Zheng, Yunkuo Li, Yujie Pan","doi":"10.1038/s41420-026-03117-8","DOIUrl":"https://doi.org/10.1038/s41420-026-03117-8","url":null,"abstract":"<p><p>Diabetic kidney disease (DKD), a prevalent microvascular complication of diabetes, is a leading cause of chronic kidney disease and end-stage renal disease. Moreover, it plays a crucial role in the morbidity and mortality of diabetic patients. Peroxisome proliferator-activated receptors (PPARs), members of the nuclear hormone receptor superfamily, are key regulators of energy homeostasis, with three distinct subtypes identified: PPARα, PPARγ, and PPARβ/δ. They regulate gene transcription associated with energy metabolism, differentiation, inflammation, and cellular development. In recent years, the increasing incidence of DKD has intensified interest in elucidating the mechanisms and roles of PPARs in DKD. Unlike previous reviews-which focused primarily on individual PPAR subtypes or isolated pathological processes-this review adopts a unique \"cell-type-specific perspective.\" It systematically elucidates the distinct roles of all three PPAR isotypes (α, γ, and β/δ) across key renal cell types (podocytes, mesangial cells, tubular cells) in DKD. We also explore the potential influence of PPAR genetic polymorphisms on DKD susceptibility. Beyond conventional review frameworks, we propose an innovative therapeutic strategy encompassing PPAR-based multi-target synergistic approaches and nanotechnology-driven cell-specific targeted therapy. This offers novel directions to overcome current therapeutic bottlenecks.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662286","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":"CX3CR1-mediated immune networks in sepsis: implications for precision therapy.","authors":"Ying Tang, Lu Jia, Yigao Liu, Zhejun Yu, Hui Chen, Ling Liu, Jie Chao, Jianfeng Xie, Haibo Qiu","doi":"10.1038/s41420-026-03102-1","DOIUrl":"https://doi.org/10.1038/s41420-026-03102-1","url":null,"abstract":"<p><p>Sepsis is a life-threatening syndrome characterized by profound immune dysregulation in response to infection, and it remains a major cause of mortality worldwide. The CX3C chemokine receptor 1 (CX3CR1) has emerged as a pivotal regulator of sepsis-induced immune dysregulation, orchestrating the proliferation, differentiation, activation, migration, and survival of various immune cell populations, including monocytes/macrophages, natural killer cells (NK), and T cells. Emerging evidence highlights that the diverse expression patterns of CX3CR1 within distinct immune cell subsets determine its dual pro-inflammatory and anti-inflammatory effects, and CX3CR1 expression level is closely correlated with patient survival in sepsis. In addition, targeted modulation of CX3CR1 in specific immune cell types has shown promising efficacy in preclinical sepsis models. This review provides a comprehensive overview of the molecular immunoregulatory networks governed by CX3CR1, its heterogenous functions across different immune subsets, and recent advances in CX3CR1-targeted therapies, highlighting cell type-specific interventions as promising strategies for precision sepsis treatment.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662258","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":"Berry-derived gold nanoparticles induce integrated ROS-mediated apoptosis, immune modulation, and transcriptomic remodeling in 4T1 triple-negative cancer cells.","authors":"Oladapo F Fagbohun, Adewale O Oladipo, Chengyu Gao, Babatunde Olawoye, Rachel S Berry, Jaylah C Captain, Olive Iragena, Xavier McDougle, Randy J Harris, Amanda Rollins, Jitcy S Joseph, Olatomide A Fadare, Russell Kincaid","doi":"10.1038/s41420-026-03023-z","DOIUrl":"https://doi.org/10.1038/s41420-026-03023-z","url":null,"abstract":"<p><p>Comprehensive molecular and phenotypic characterization of tumor models is still needed for a robust understanding of breast cancer mechanisms and therapies. Here, we explore the genome, transcriptome, and proteome of treated and untreated 4T1 triple-negative breast cancer cells to integrate genomic vulnerabilities and mutational profiling with novel treatment-induced delivery, signaling, and apoptotic responses. Nanoencapsulation (AuNPs) of berry-derived polyphenolic compounds was influenced by limited clinical use due to poor stability and bioavailability. Several physicochemical characterizations employed include TEM, FTIR, and targeted UPLC/MS-QQQ assays. We identified significant mutations to breast cancer-related tumor suppressor genes (TP53, BRCA2, BARD1, CDH1, NF1, and CHEK2) and deciphered the functional consequences leveraging the higher throughput Illumina NovaSeq X and NextSeq sequencing and the highly accurate predictive power of AlphaFold. We found ~5,700,000 single-nucleotide variations (SNVs) and 329448 indels, achieving an important upgrade over existing literature data. Multiple sequence alignment with WT mouse and human protein sequences demonstrated that mutations present in 4T1 cells are within highly conserved motifs of key tumor suppressors, emphasizing their relevance to human breast cancer biology. Key findings from differentially expressed gene enrichment analyses (GSEA) revealed positive gene enrichments of DNA repair regulators and TGF-β signaling, while having negative enrichments of cell adhesion, cadherin and MAPK signaling via PI3K/AKT/MAPK/Wnt pathways, potentially influencing apoptosis and immune evasion intrinsic to cancer. Notably, decreased expression of PIK3CG, PALLD, PTPRZ1, and CDH8 and increased expression of SEMA6C, WWOX, NHEJ1, and MAML3 suggested suppression of epithelial-to-mesenchymal transition (EMT) and metastatic potential. Further assessment of immunohistochemical, immunofluorescent, and flow cytometric data revealed that berry-derived nanoparticles are associated with the modulation of oncogenic transcription factors and linked to induced caspase-dependent execution-phase ROS-mediated apoptosis through pPAK1^Thr212 dephosphorylation, downregulation of pPI3K^{p85αγ(Tyr467/199)}/pAKT1^Thr450/mTOR signaling, and modulation of pJAK3^Tyr785/STAT3 pathway supporting transcriptomic and transcriptional reprogramming of 4T1 treated cells. Together, our findings uncover a new strategy to capture berry-derived polyphenols required to regulate apoptosis, autophagy, immune response, and metastasis-related gene networks in breast cancer, thereby underscoring the therapeutic potential of functionalized AuNPs as delivery platforms for dietary phytochemicals.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653881","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":"NAT10 promotes cisplatin resistance and immune escape by increasing the expression of DUSP1 and PD-L1 in gastric cancer.","authors":"Lilin Qian, Wenrong Gao, Xinyi Wang, Shuqi Cui, Xiaoqi Han, Xia Xu, Jihui Jia, Zhifang Liu","doi":"10.1038/s41420-026-03107-w","DOIUrl":"https://doi.org/10.1038/s41420-026-03107-w","url":null,"abstract":"<p><p>Developing resistance to chemotherapy drugs and evading the killing effect of the immune system are the main obstacles in the clinical treatment of gastric cancer. However, the potential mechanism remains poorly understood. N-acetyltransferase 10 (NAT10) catalyzes the N4-acetylcytidine (ac4C) modification of mRNA and is associated with tumor occurrence, development and chemotherapy resistance. Here, we observed that elevated NAT10 levels promote cisplatin chemoresistance in gastric cancer cells. On the contrary, knockdown of NAT10 enhances the sensitivity of cisplatin-resistant gastric cancer cells to cisplatin, both in vitro and in vivo. Mechanistically, NAT10 binds to DUSP1 mRNA and catalyzes its ac4C modification at positions C327, C330, and C331 within the coding sequence (CDS) region, thereby enhancing the stability of DUSP1 mRNA and increasing the abundance of DUSP1 protein. Furthermore, NAT10 mediates resistance to cisplatin-induced apoptosis through DUSP1 via the JNK and ERK signaling pathways. Additionally, NAT10 can upregulate PD-L1 expression via FOSB. The combination of a NAT10 inhibitor and an anti-PD-1 antibody synergistically enhances the antitumor efficacy against cisplatin- resistant gastric cancer cells in murine models. Taken together, these findings offer novel insights into the role and mechanism of NAT10 in the crosstalk between cisplatin chemoresistance and immunosuppression in gastric cancer. NAT10 thus holds promise as a highly attractive target, with the potential to synergize with PD-1-based immunotherapy to reverse cisplatin resistance in gastric cancer.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644260","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}