Cell Death Discovery最新文献

{"title":"Bridging the marrow: a co-culture-platform of leukemia cells and MS5-derived stromal cells or adipocytes.","authors":"Julia Zinngrebe, Elena Dorothea Brenner, Ferdinand Schlichtig, Ulrich Stifel, Daniel Tews, Jana Falk, Dominik Schlotter, Rahel Fitzel, Lüder-Hinrich Meyer, Klaus-Michael Debatin, Pamela Fischer-Posovszky","doi":"10.1038/s41420-025-02631-5","DOIUrl":"10.1038/s41420-025-02631-5","url":null,"abstract":"<p><p>In the context of acute lymphoblastic leukemia (ALL), the bone marrow microenvironment (BMM) plays a crucial role in providing pro-survival signals, as evident from the rapid spontaneous cell death observed in ex-vivo cultures of primary ALL cells. Among the diverse cell types within the BMM, bone marrow adipocytes (BMAd) exhibit significant plasticity and can constitute a substantial part of the BMM, especially during ALL therapy. However, conflicting data on the interaction between ALL cells and adipocytes have been reported, potentially arising from variations in culture systems and conditions. Our study aimed to establish a chemically defined co-culture system of leukemia cells combined with either bone marrow (BM)-derived stromal cells or adipocytes. Established B-precursor ALL cell lines, patient-derived ALL xenografts (PDX), and murine BM-derived MS5 stromal cells and adipocytes were used as model systems. Fetal calf serum and factors included in the adipogenic media significantly impacted leukemia cell viability and proliferation. Thus, we implemented a washing procedure and suitable, chemically defined media conditions into our co-culture platform. In general, ALL cell lines survived and proliferated on both stromal cells and adipocytes, whereas PDX cells exhibited a pronounced survival advantage on stromal cells compared to adipocytes. Intriguingly, the presence of adipocytes sensitized cell lines and PDX cells to chemotherapy with anthracyclines or dexamethasone when compared to co-cultures with stromal cells. Thus, utilizing the well-established MS5 cell line together with the optimized culture conditions in our co-culture system provides a reliable, open-access platform for investigating intricate interactions between bone marrow stromal cells, adipocytes, and leukemia cells.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"366"},"PeriodicalIF":7.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788373","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":"Inhibition of ferroptosis in inflammatory macrophages alleviates intestinal injury in neonatal necrotizing enterocolitis.","authors":"Leiting Shen, Jiayu Chen, Jinfa Tou","doi":"10.1038/s41420-025-02665-9","DOIUrl":"10.1038/s41420-025-02665-9","url":null,"abstract":"<p><p>Neonatal necrotizing enterocolitis (NEC) is a severe gut disease primarily affecting preterm infants, driven significantly by inflammatory macrophages. This study combined bioinformatics (single-cell/tissue RNA sequencing) and experiments to identify key macrophage changes in NEC. Analysis revealed substantial macrophage infiltration in NEC tissues. These macrophages were highly inflammatory and strongly linked to cell death pathways (ferroptosis, pyroptosis, apoptosis), with scores significantly higher than controls and correlating with inflammation. In vitro, LPS-stimulated inflammatory macrophages showed elevated ferroptosis, evidenced by cell rupture, death, increased ACSL4, decreased GPX4, iron overload, lipid peroxidation, and heightened cytokine release. Critically, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) reversed these effects. While LPS alone didn't kill intestinal epithelial cells, supernatant from LPS-stimulated macrophages significantly increased intestinal epithelial cell death. Fer-1 inhibition of macrophage ferroptosis prevented this epithelial damage. In vivo, a mouse NEC model (induced by hypersomolar feeding, hypoxia, cold) displayed macrophage infiltration, inflammation, and elevated ferroptosis markers. Intraperitoneal Fer-1 administration improved intestinal injury in NEC mice. This study demonstrates that macrophage ferroptosis is a critical driver of NEC inflammation and tissue damage. Inhibiting ferroptosis with Fer-1 effectively reduces both macrophage death and subsequent intestinal epithelial injury, mitigating NEC progression. These findings highlight macrophage ferroptosis as a key therapeutic target for NEC, offering a foundation for new treatment strategies.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"365"},"PeriodicalIF":7.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12325787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788374","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":"Hallmarks and mechanisms of cellular senescence in aging and disease.","authors":"Amir Ajoolabady, Domenico Pratico, Suhad Bahijri, Basmah Eldakhakhny, Jaakko Tuomilehto, Feng Wu, Jun Ren","doi":"10.1038/s41420-025-02655-x","DOIUrl":"10.1038/s41420-025-02655-x","url":null,"abstract":"<p><p>Cellular senescence, often referred to simply as \"senescence\", is a complex intracellular process with diverse biological, physiological, and pathological roles. Biologically, it is essential for embryogenesis and development. Physiologically, senescence acts as a safeguard against tumorigenesis by preventing the proliferation of damaged or defective cells. However, persistent activation of senescence can contribute to various pathological conditions, particularly those associated with aging, cancer, and other chronic diseases such as liver and pulmonary diseases. Growing evidence links aging to heightened activation of cellular senescence, leading to the accumulation of senescent cells. Here in this perspective, we aim to decipher the latest molecular mechanisms and regulatory pathways of cellular senescence in the context of aging and aging-related diseases. Additionally, we discuss emerging research directions, highlighting current limitations and gaps in the field. Addressing these challenges may not only advance our understanding of senescence but also uncover new therapeutic opportunities.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"364"},"PeriodicalIF":7.0,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12322153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783614","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":"CDK inhibitors promote neuroblastoma cell differentiation and increase sensitivity to retinoic acid-a promising combination strategy for therapeutic intervention.","authors":"Fatemeh Shokraie, Larissa Lechermeier, Pia Bordihn, Philipp Kaps, Steffen Möller, Anna Sophie Schulz, Björn Schneider, Dirk Koczan, Samira Khanipour Roshan, Holger N Lode, Carl-Friedrich Classen, Olga Hahn, Sascha Troschke-Meurer, Claudia Maletzki","doi":"10.1038/s41420-025-02637-z","DOIUrl":"10.1038/s41420-025-02637-z","url":null,"abstract":"<p><p>The rarity of recurrent somatic mutations poses a challenge for the targeted treatment of neuroblastoma (NB). Differentiation therapy is an encouraging prospect, with cyclin-dependent kinase inhibitors (CDKis) representing a promising avenue for promoting NB differentiation. This study investigated three CDKis (abemaciclib, fadraciclib, and dinaciclib) alone or combined with retinoic acid (RA) to assess the effects on morphology, growth, gene expression, and the induction of immunogenic cell death in NB cell lines with (LAN-1 and CHLA-90) and without (CHLA-172) MYCN amplification. All cell lines demonstrated sensitivity to CDK inhibition. Notably, low-dose abemaciclib promoted cellular differentiation, as evidenced by the emergence of stromal-like morphological features and upregulation of the differentiation markers STMN4 and ROBO2. Treatment with abemaciclib or fadraciclib led to the upregulation of calnexin and holocytochrome C, which are part of the global stress response, along with the protein p27, which arrests the cell cycle. Molecularly, CDKis sensitivity correlated with an increased CDK4-specific copy number, along with a partial deletion of CDKN2a in two cases (LAN-1, CHLA-172). The addition of RA augmented the effects of the monotherapy, particularly in LAN-1 cells, in both 2D and 3D culture, and both treatments triggered immunogenic cell death, evidenced by calreticulin translocation. Transcriptomic analysis of LAN-1 and CHLA-90 cells revealed that genes deregulated by monotherapy (fadraciclib or RA) were re-regulated in the presence of the second drug. Combination therapy significantly downregulated CRABP2 and CYP26B1, both of which are involved in RA metabolism and its degradation. Furthermore, CCNE2, MYBL2, and MCM4 were strongly suppressed in the fadraciclib/RA combination, confirming the induction of cell cycle arrest. CDKi treatments promote NB differentiation via ER stress, with cytotoxicity enhanced by RA co-treatment. This may increase NB immunogenicity and support immunotherapy eligibility.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"363"},"PeriodicalIF":7.0,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12318081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768455","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":"Panobinostat potentiates adagrasib-induced cell death by triggering autophagy in human non-small cell lung cancer.","authors":"Hui Lu, Wenying Fu, Yiqun Xia, Ying Yan, Chongchong Shu, Yinghua Chen, Chenxin Xu, Peisen Zheng, Xin Shen, Ri Cui, Peng Zou, Daoyong Ni","doi":"10.1038/s41420-025-02657-9","DOIUrl":"10.1038/s41420-025-02657-9","url":null,"abstract":"<p><p>Adagrasib, a KRASG12C inhibitor, recently received accelerated approval from the US FDA for the treatment of patients diagnosed with KRASG12C-mutated non-small cell lung cancer. Although adagrasib has demonstrated excellent clinical efficacy and good safety, the molecular mechanism underlying the antitumor activity of adagrasib remains elusive. Here, we report that adagrasib treatment markedly inhibited the growth of cells harboring the KRASG12C mutation, whereas the non-KRASG12C cell lines H1299 and PC-9 were also sensitive to adagrasib, indicating that adagrasib exerted off-target effects. Mechanism studies indicated that adagrasib treatment reduced the level of NRF2 via upregulating its ubiquitination, and NRF2 overexpression can reverse the adagrasib-induced cell death in H23 and H1299 cells. Furthermore, adagrasib treatment significantly increased the cellular ROS level and thereby activating autophagy and AKT signaling pathways in H23 and H1299 cells. Importantly, combination of adagrasib with panobinostat demonstrated enhanced antitumor activity in vitro and in vivo. Overall, our data elucidate a novel mechanism of adagrasib, which will be critical for the clinical application of adagrasib.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"360"},"PeriodicalIF":7.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764607","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":"HADHA-mediated regulation of JAK/STAT3 signaling in glioblastoma: a metabolic-epigenetic axis.","authors":"Kan Wang, Yifei Xiao, Jinxin Wan, Yuanqi Chu, Ruipeng Zheng, Fengjun Lv, Guang Yang, Mingchun Yang, Haitao Ge, Yuwen Song, Yu Cheng","doi":"10.1038/s41420-025-02660-0","DOIUrl":"10.1038/s41420-025-02660-0","url":null,"abstract":"<p><strong>Astract: </strong>Glioblastoma multiforme (GBM) is one of the most aggressive forms of brain cancer, characterized by rapid growth and resistance to conventional therapies. This study investigates the role of HADHA, a key enzyme in fatty acid β-oxidation, in the progression of GBM. we show that the overexpression of HADHA in GBM correlates with a poor prognosis in patients and plays a role in promoting tumor growth and invasion. Mechanistically, HADHA regulates the JAK/STAT3 signaling pathway through modulation of H3K27ac histone acetylation. Knockdown of HADHA results in decreased acetyl-CoA levels, leading to reduced H3K27ac modification and subsequent inhibition of JAK/STAT3 activation. Furthermore, we show that the small molecule JIB-04, which targets HADHA, inhibits GBM cell proliferation and invasion both in vitro and in vivo. Our findings highlight the importance of targeting metabolic enzymes in cancer therapy and suggest that HADHA could represent a potential new therapeutic target for GBM. By targeting the metabolic-epigenetic pathway, this strategy presents a promising approach for treating this devastating disorder.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"361"},"PeriodicalIF":7.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764605","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":"DCAF13 is essential for mouse uterine function and fertility.","authors":"Qianhui Zhou, Xiaohui Li, Ningjing Wang, Liang Zhang, Enhui Jiang, Kaixuan Wang, Xingyu Yan, Cong Zhang","doi":"10.1038/s41420-025-02583-w","DOIUrl":"10.1038/s41420-025-02583-w","url":null,"abstract":"<p><p>The incidence of female infertility is a growing worldwide concern and a leading cause of population decline. Therefore, understanding the pathogenesis of infertility is of utmost importance. DDB1 and CUL4 Associated Factor 13 (DCAF13) is a significant component of the CRL4 E3 ubiquitin ligase complex responsible for recognizing substrates and degrading them after polyubiquitylation. DCAF13 has been implicated in oocyte and embryo development, but its role in the uterus remains elusive. To investigate its function, we generated Dcaf13 conditional knockout (cKO) mice and discovered that the uteri of cKO mice became smaller and thinner as they mature, and the embryos were unable to implant, leading to infertility. Mechanistically, we detected aberrant expression of estrogen and progesterone receptors, along with dysregulation of estrogen- and progesterone-responsive genes in the endometrium. This led to insufficient proliferation of endometrial cells in mice. RNAseq analysis revealed an overall increase in transcription of methylation-related genes, including SUV39H2, leading to higher H3K9me3 levels and consequently hindered cell proliferation in the uterus. Furthermore, DCAF13 knockdown resulted in elevated intracellular H3K9me3 levels. In conclusion, these findings suggest that DCAF13 is essential for maintaining the structure of the uterus and fertility. This study potentially contributes to the development of new strategies aimed at improving female reproductive health.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"359"},"PeriodicalIF":7.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764604","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":"Heparan sulfate binding protein treatment ameliorates neuropathology and behavioral abnormalities in mucopolysaccharidosis IIIB mice.","authors":"Serenella Anzilotti, Melania Scarcella, Mariangela Ciampa, Noemi Di Muraglia, Camilla Anastasio, Chiara Fiorentino, Federica Rossin, Luigi Avallone, Giuseppe Pignataro, Luigi Michele Pavone, Valeria De Pasquale","doi":"10.1038/s41420-025-02648-w","DOIUrl":"10.1038/s41420-025-02648-w","url":null,"abstract":"<p><p>Mucopolysaccharidosis IIIB (MPS IIIB) is a metabolic neurodegenerative disorder caused by a deficiency of the lysosomal enzyme α-N-acetylglucosaminidase (NAGLU), which is involved in the degradation of heparan sulfate (HS). Affected patients exhibit progressive neurodegeneration, behavioral disturbances, and a shortened lifespan. Currently, there is no effective treatment for MPS IIIB. We have recently developed a new therapeutic strategy based on the use of the HS-binding protein NK1, a spliced variant of hepatocyte growth factor. Here, we demonstrate that treating Naglu^-/- mice with recombinant NK1 ameliorates neuropathology by reducing HS storage, lysosomal dysfunction, autophagy imbalance, and neuroinflammation in the cortex and hippocampus of MPS IIIB mouse brains. Furthermore, we found that recombinant NK1 treatment improves cognitive behavior and motor activity in Naglu^-/- mice, as assessed using open field, object recognition, and T-maze tests. Our findings suggest that recombinant NK1 is a promising candidate for the treatment of MPS IIIB and other lysosomal storage diseases associated with central nervous system dysfunction.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"362"},"PeriodicalIF":7.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12316897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764606","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":"Redox mechanism of glycerophospholipids and relevant targeted therapy in ferroptosis.","authors":"Shuwei Chang, Minghui Zhang, Chang Liu, Mingyu Li, Yuefen Lou, Hexin Tan","doi":"10.1038/s41420-025-02654-y","DOIUrl":"10.1038/s41420-025-02654-y","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent form of regulated cell death driven by redox dysregulation, is defined by iron overload, reactive oxygen species overproduction, and subsequent peroxidation of polyunsaturated fatty acid-containing phospholipids, notably glycerophospholipids. This review comprehensively delineates the enzymatic such as lipoxygenases and non-enzymatic including Fenton reaction pathways governing glycerophospholipid peroxidation. Furthermore, we systematically dissect fine regulation of iron ions, including absorption, transport, and redox state transition. Given pathophysiological relevance of ferroptosis to numerous diseases, especially neurodegenerative disorders and various cancers, we evaluate emerging therapeutic strategies targeting key ferroptosis nodes, with a primary focus on the key enzymes involved in lipid peroxidation, transferrin receptor-mediated endocytosis mechanism and traditional Chinese medicine. Our work provides a direction for advancing ferroptosis research and developing combinatorial therapies that synergize ferroptosis induction with conventional treatments.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"358"},"PeriodicalIF":7.0,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12314118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759217","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":"Targeting iron regulatory protein 2 (IRP2) to disrupt iron metabolism enhances radiosensitivity through mitochondrial dysfunction in breast cancer cells.","authors":"Ye Yeong Jeong, Jieon Hwang, Areum Park, Sungmin Cho, Inyoung Cho, Soseul Won, You Me Shin, Sung Eun Kim, Chan Hoon Maeng, Jaemoon Yang, Minhee Ku, Hyuk Lee, Sang Joon Shin","doi":"10.1038/s41420-025-02653-z","DOIUrl":"10.1038/s41420-025-02653-z","url":null,"abstract":"<p><p>Iron regulatory protein (IRP2) plays a key role in regulating iron metabolism and enables cell survival by activating mitochondrial function. Targeting IRP2 to disrupt iron homeostasis is a promising strategy for enhancing the efficacy of cancer treatments. Depletion of IRP2 in breast cancer (BC) cells is associated with sensitivity to radiation therapy (RT), and inhibition of IRP2 prior to RT significantly reduces cell viability compared with radiation treatment alone. This combined therapeutic effects of IRP2 inhibition and radiation treatment were observed in parental and radioresistant cancer cells, significantly enhancing the proportion of cell death. In conclusion, this study proposes that the genetic or pharmacological inhibition of IRP2 in BC cells may serve as a novel therapeutic strategy for increasing radiosensitivity and overcoming resistance by inducing mitochondrial dysfunction.</p>","PeriodicalId":9735,"journal":{"name":"Cell Death Discovery","volume":"11 1","pages":"357"},"PeriodicalIF":7.0,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12314050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759218","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}