Human Cell最新文献

{"title":"Establishment of human histiocytic sarcoma organoids dependent on the SHH/YAP pathway.","authors":"Yusuke Yoshimura, Keiichi Yoshida, Yukiko Matsuoka, Satoru Sasagawa, Noriko Nagamine, Yoji Kukita, Ryota Miyamoto, Rie Suzuki, Hironari Tamiya, Shigeki Kakunaga, Toshinari Yagi, Takuya Terakawa, Yuma Tada, Takafumi Yokota, Jun Ishikawa, Sho Nakai, Yoshinori Imura, Seiji Okada, Ken-Ichi Yoshida, Satoshi Takenaka, Toru Wakamatsu","doi":"10.1007/s13577-025-01308-6","DOIUrl":"https://doi.org/10.1007/s13577-025-01308-6","url":null,"abstract":"<p><p>Histiocytic sarcoma is an extremely rare and aggressive malignant neoplasm characterized by immunophenotypic features of mature histiocytes. The mechanisms underlying its malignant transformation remain poorly understood; consequently, the development of effective therapies remains limited. Resected histiocytic sarcoma specimens were cultured using a modified air-liquid interface organoid method, serially passaged, and xenografted into NOD-scid IL2Rgnull mice. Tumors formed by xenografted organoids retained histological and genetic similarities with the original tumor. Genomic analysis revealed the activation of the Sonic Hedgehog signaling pathway and amplification of Yes-associated protein 1, a key effector of the Hippo pathway. Accordingly, we evaluated the sensitivity of the organoids to the Sonic Hedgehog inhibitor vismodegib and Yes-associated protein 1 inhibitor verteporfin, both of which demonstrated potent in vitro antitumor activity in organoid cultures. This model offers a valuable preclinical platform for investigating the molecular pathology of this rare malignancy and accelerating the development of targeted therapies.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"175"},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-cell transcriptome analysis highlights a critical role of ATG5 for endothelial cells in diabetic nephropathy.","authors":"Yun Zhang, Lishuang Che, Hanyuan Gao, Quanzuan Zeng, Jiequn Zhang, Yanling Zheng, Yuangen Li, Xiaoqing Chen","doi":"10.1007/s13577-025-01302-y","DOIUrl":"https://doi.org/10.1007/s13577-025-01302-y","url":null,"abstract":"<p><p>This study analyzed diabetic nephropathy (DN)-related single-cell RNA sequencing (scRNA-seq) data from public databases and dissected the mechanism by which the sirtuin 1 (SIRT1)/autophagy-related 5 (ATG5) axis mediates high glucose (HG)-induced human renal glomerular endothelial cell (HRGEC) injury. The endothelium cluster was analyzed with DN-related scRNA-seq data (GSE131882 and GSE264268). HG-induced HRGEC injury was assessed by detecting cell viability, LDH release, apoptosis, EMT, and autophagy. SRT1720 was used to activate SIRT1 in cell models and STZ-induced mouse models. Renal dysfunction and pathological injury were assessed by detecting urinary albumin, serum creatinine, and BUN levels and performing histopathological staining (H&E, PAS, Masson, and TUNEL). Analysis of the endothelium cluster discovered that the autophagy pathway in the endothelial cluster was suppressed in early-stage DN patients and mice. Moreover, HG induced cell apoptosis and EMT in HRGECs, along with elevated acetylated levels of ATG5 and decreased protein levels of ATG5. SRT1720 decreased apoptosis, EMT, and elevated autophagic flux in HG-induced HRGECs, as well as improved renal function and histopathological changes, reduced EMT, and elevated autophagy in DN mouse models. However, Atg5 silencing reversed SRT1720-mediated alterations in these parameters. The SIRT1/ATG5 axis-dependent HRGEC autophagy restoration exerts a protective effect on the kidney during DN, offering a scientific ground for developing therapeutic strategies for DN based on autophagy regulation.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"174"},"PeriodicalIF":3.1,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omic analysis constructs ferroptosis subtypes and risk signature and reveals that PEBP1 is an important tumor suppressor in kidney cancer.","authors":"Shuaiqi Chen, Xizi Cheng, Zeyu Li, Huijun Fan, Xiangdong Xue, Kuo Ma, Jingxian Li, Feng Zhu","doi":"10.1007/s13577-025-01303-x","DOIUrl":"https://doi.org/10.1007/s13577-025-01303-x","url":null,"abstract":"<p><p>Ferroptosis, an iron-dependent type of regulated cell death driven by excessive lipid peroxidation, plays an important role in natural tumor suppression. In this study, we identified 23 ferroptosis-related genes associated with prognosis in kidney cancer datasets. Based on the expression profiles of these genes, we classified kidney cancer into four distinct subtypes and constructed a 9-gene risk score to predict the prognosis of patients. Our analysis revealed that patients classified into group III and those in the low-risk group demonstrated significantly better survival probability. Moreover, the risk score exhibited strong predictive accuracy for the prognosis of kidney renal clear-cell carcinoma (KIRC) patients. Among the identified genes, PEBP1 showed elevated expression in both subtype III and the low-risk group, suggesting that it may act as a critical tumor suppressor. To further evaluate this, we examined PEBP1 expression patterns and their clinical correlations using TCGA-KIRC and KIRP cohorts. The results indicated that PEBP1 deletion was strongly associated with poor prognosis, while reduced PEBP1 expression correlated with advanced disease progression in both KIRC and KIRP patients. Functional enrichment analysis suggested that PEBP1 may be involved in pathways related to fatty acid metabolism and oxidative phosphorylation. Experimental validation supported these findings, showing that PEBP1 overexpression suppressed the proliferation and migration of kidney cancer cells. Additionally, PEBP1 promoted the accumulation of lipid reactive oxygen species (ROS), an effect that was reversed by a ferroptosis inhibitor. Conversely, silencing PEBP1 counteracted the lipid ROS induced by RSL4, a ferroptosis activator. In summary, our results demonstrate that PEBP1 functions as a potential tumor suppressor in kidney cancer and may serve as a promising prognostic biomarker and therapeutic target.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"173"},"PeriodicalIF":3.1,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240253","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging role of the E3 ubiquitin ligase RNF114 in health and disease.","authors":"Qian Wang, Shihan Cao, Zhenzhen Sun, Zhanjun Jia, Shiwei Yang","doi":"10.1007/s13577-025-01305-9","DOIUrl":"https://doi.org/10.1007/s13577-025-01305-9","url":null,"abstract":"<p><p>Ubiquitination plays important roles in various biological processes and diseases by affecting the subcellular localization, function, and degradation of substrates. Multiple ubiquitin-associated enzymes jointly mediate the binding of ubiquitin to substrates. Over the past few decades, numerous E3 ubiquitin ligases, including RING finger protein 114 (RNF114), have been well studied. Research has revealed the involvement of RNF114 in various biological processes, including embryonic development, the cell cycle, genome stability, the immune response, and osteoclastogenesis. Additionally, RNF114 is implicated in multiple diseases, such as viral infections, psoriasis, liver fibrosis, and cancer. This review recapitulates the most recent advances regarding RNF114 and provides possible directions for future research.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"172"},"PeriodicalIF":3.1,"publicationDate":"2025-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elucidating the risk factors and oncogene drivers of acute myeloid leukemia.","authors":"Daniel Ruben Akiola Sanya, Djamila Onésime","doi":"10.1007/s13577-025-01294-9","DOIUrl":"https://doi.org/10.1007/s13577-025-01294-9","url":null,"abstract":"<p><p>The hematopoietic system is critical for maintaining physiological homeostasis but is also implicated in various pathologies. The magnitude of hematopoietic responses to perturbations or diseases exhibits significant inter-individual variability, underscoring the need to identify predictors and determinants of blood responsiveness in humans. These reactions are shaped not only by genetic factors but also by epigenetic modifications and environmental effects. Elucidating baseline predictors of hematopoietic responses and their molecular underpinnings is of particular interest in acute myeloid leukemia (AML), given their potential to inform malignancy immunotherapy. Due to limited understanding of the cellular and molecular mechanisms driving diverse AML subtypes in pediatric and adult patients, coupled with an increasing prevalence of refractory or relapsed hematological malignancies, this review highlights underexplored prognostic biomarkers, their molecular mechanisms, and their potential clinical utility in optimizing therapeutic strategies for improved patient survival. It examines recent advances in AML research and vaccine development, focusing on efforts to address highly aggressive and rare AML subtypes driven by aberrantly activated transcription factors. The review also addresses clinical implications for overall survival and treatment response, as well as promising vaccine candidates. Additionally, it highlights newly identified mutations and high-risk molecular markers that could enhance risk stratification for early disease progression, identifying patients who may benefit from allogeneic stem cell transplantation or enrollment in clinical trials.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"171"},"PeriodicalIF":3.1,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZWINT down-regulated by miR-495-3p inhibited lung metastasis of breast cancer by blocking p38 MAPK signaling pathway activation.","authors":"Ming-Tao Shao, Wei-Wen Li, Yong Li, Ping Chen, Shuai-Shuai Yu, Wen-Jie Lu, Chun-Mei Chen, Yan Dong, Yi-Wen Zhang, Qun-Chen Zhang","doi":"10.1007/s13577-025-01301-z","DOIUrl":"10.1007/s13577-025-01301-z","url":null,"abstract":"<p><p>Breast cancer metastasis is the primary cause of patient mortality, yet effective therapeutic targets remain limited. Building on our prior identification of ZWINT as a prognostic marker linked to metastasis, this study defines its critical functional role and regulatory mechanism. Multi-omics analysis revealed a strong association between ZWINT expression and metastatic processes across breast cancer subtypes. Functionally, ZWINT knockdown significantly inhibited breast cancer cell migration and invasion in vitro and dramatically reduced lung metastasis in vivo. Mechanistically, we discovered that miR-495-3p directly targets and suppresses ZWINT expression, and this miR-495-3p/ZWINT axis acts through inhibiting p38 MAPK pathway activation to suppress metastatic progression in vitro. Our findings demonstrate that ZWINT drives breast cancer metastasis and is negatively regulated by miR-495-3p. The newly identified miR-495-3p/ZWINT/p38 MAPK axis may provide a promising therapeutic target for suppressing breast cancer progression.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"170"},"PeriodicalIF":3.1,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12496286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Podocytes in health and disease: from development to regeneration.","authors":"Yusuke Nishimura","doi":"10.1007/s13577-025-01296-7","DOIUrl":"https://doi.org/10.1007/s13577-025-01296-7","url":null,"abstract":"<p><p>Podocytes are highly specialized epithelial cells that are essential for maintaining the glomerular filtration barrier. They originate from the metanephric mesenchyme during kidney development, with differentiation tightly regulated by transcription factors, such as Wt1, MafB, and Lmx1b, as well as signaling pathways, including Wnt and Notch. Mature podocytes form intricate foot processes and slit diaphragms, coordinating membrane proteins, such as nephrin and podocin, with the actin cytoskeleton to ensure selective filtration. Owing to their limited regenerative capacity, podocyte injury caused by genetic mutations, mechanical stress, metabolic disorders, or inflammation leads to proteinuria, glomerulosclerosis, and the progression of chronic kidney disease. Recent studies have elucidated diverse injury mechanisms, including apoptosis, necroptosis, ferroptosis, and cytoskeletal dysregulation, highlighting aging and lipid metabolism as key modulators of podocyte vulnerability. Advances in stem cell technology and kidney organoids have enabled the modeling of podocyte development and disease, paving the way for regenerative strategies. This review provides a comprehensive overview of podocyte biology, injury mechanisms, and emerging therapeutic approaches, emphasizing translational opportunities for protecting and restoring podocyte function in kidney diseases.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"169"},"PeriodicalIF":3.1,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL14 knockdown augmented the polarization of M2-like macrophages to promote acute myeloid leukemia progression.","authors":"Meng Wang, Zhibin Xie, Yuanyuan Tan, Yan Zhou, Siyi Wang, Pingping Zhang, Jiajia Li","doi":"10.1007/s13577-025-01300-0","DOIUrl":"https://doi.org/10.1007/s13577-025-01300-0","url":null,"abstract":"<p><p>Within the m6A methyltransferase complex, methyltransferase-like 14 (METTL14) constitutes a pivotal component. This study aims to elucidate the role of METTL14 in macrophage differentiation and its involvement in the progression of acute myeloid leukemia (AML) through the modulation of programmed cell death-ligand 1 (PD-L1) expression in M2-like macrophages. The expression levels of METTL14 in M1-like and M2-like macrophages were quantified using real-time quantitative polymerase chain reaction (QRT-PCR). Macrophage differentiation in THP-1 cells was induced via treatment with phorbol 12-myristate 13-acetate (PMA), followed by lentiviral-mediated overexpression or knockdown of METTL14. Changes in the expression of CD86, iNOS, Arg-1, and CD206 were evaluated. The effects of METTL14 knockdown and overexpression on macrophage differentiation, M2 macrophage proliferation, and apoptosis was assessed. AML cells were co-cultured with M2 macrophages subjected to either METTL14 knockdown or overexpression, and subsequent changes in AML cell proliferation, apoptosis, migration, invasion, and m6A methylation levels were investigated. The expression of METTL14 mRNA was elevated in M1-like macrophages. Knockdown of METTL14 resulted in a significantly reduction in the expression of M1 markers, such as CD86 and iNOS, while concurrently increasing the expression of M2 markers, including Arg-1 and CD206. Additionally, the depletion of METTL14 facilitated the proliferation of M2-like macrophages, inhibited apoptosis, and decreased phagocytic capacity. Conversely, overexpression of METTL14 yielded opposite outcomes. Co-culture experiments demonstrated that M2-like macrophages with METTL14 knockdown significantly promoted the proliferation of AML cell, suppressed apoptosis, and enhanced migration and invasion. Concurrently, cellular m6A levels were elevated. Treatment with anti-PD-L1 partially reversed the effects of METTL14 knockdown. These findings suggest that METTL14 may enhance the proliferation of AML cells while inhibiting apoptosis by influencing macrophage differentiation and modulating macrophage function, with these effects being associated with YTHDF1 and PD-L1.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"168"},"PeriodicalIF":3.1,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145201809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hofbauer cell alterations and potential role in the pathophysiology of HELLP syndrome.","authors":"Ayano Ezaki, Akihito Sagara, Yoshihiro Komohara, Cheng Pan, Hiromu Yano, Shukang Zhao, Mayuko Yamamoto, Anri Imamura, Hinano Akita, Jie Su, Ren Shirotani, Tomoka Takahashi, Daiki Yoshii, Yukio Fujiwara, Masahiro Yamamoto, Munekage Yamaguchi, Eiji Kondoh","doi":"10.1007/s13577-025-01297-6","DOIUrl":"https://doi.org/10.1007/s13577-025-01297-6","url":null,"abstract":"<p><p>HELLP syndrome, a severe pregnancy complication characterized by hemolysis, elevated liver enzymes, and low platelet count, is a subtype of preeclampsia (PE). However, its rapid onset and unique clinical features suggest distinct underlying mechanisms. Although Hofbauer cells are essential for maintaining immune homeostasis, their involvement in HELLP syndrome remains unclear. We conducted transcriptomic analysis of public data sets to assess macrophage-associated gene expression in placentas from control, PE, and HELLP cases. Immunohistochemistry and image analysis were performed on formalin-fixed paraffin-embedded placental tissues to quantify macrophage density and size, and electron microscopy was conducted to evaluate ultrastructural features. Gene expression analysis revealed a significant reduction in AIF1 (Iba1) and CD163 expression in PE placentas, while CD163 expression was relatively preserved in HELLP. Immunohistochemistry confirmed decreased Hofbauer cell density in PE placentas, whereas enlarged Hofbauer cells with increased rough endoplasmic reticulum, suggesting enhanced activation status, were seen in HELLP. Hofbauer cells exhibit distinct morphological and molecular changes in HELLP syndrome compared with PE, which implicates their potential involvement in the pathophysiology of HELLP. These findings provide new insights into the fetal immune environment in pregnancy-related hypertensive disorders.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"167"},"PeriodicalIF":3.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eucommia ulmoides (Duzhong) extract alleviates cerebral stroke by inhibiting ferroptosis-related gene DNA Damage-Inducible Transcript 4 (DDIT4) expression.","authors":"Xin Qi, Mengyuan Deng, Minhong Li, Wenjia Ma, Yangbo Zhou","doi":"10.1007/s13577-025-01298-5","DOIUrl":"https://doi.org/10.1007/s13577-025-01298-5","url":null,"abstract":"<p><p>Cerebral stroke is an acute cerebrovascular disease, which is characterized by significant morbidity, death, and disability rate. Ischemic stroke is more than hemorrhagic stroke and accounts for 60-70% of all strokes. The present study explored the mechanisms of Eucommia ulmoides extract (EUE) in the treatment of ischemic stroke. Middle cerebral artery occlusion (MCAO) mouse models and oxygen and glucose deprivation (OGD) SH-SY5Y cell models were constructed to mimic ischemic stroke, and mice and cells were treated with gradient concentrations of EUE. The neurological function and brain tissue damage in mice were assessed using multiple parameters. Then the iron contents in cerebral tissue samples and neuronal cells were examined, and the expression levels of reactive oxygen species-related indicators and iron metabolism-related proteins were detected. EUE alleviated the ferroptosis process within cerebral tissue samples of MCAO mice and OGD-triggered neuronal cells, thereby mitigating neurological function and brain tissue damage by activating PI3K/Akt pathway. The target drug genes of EUE were searched by network pharmacology and molecular docking and found that the ferroptosis-related gene DDIT4 is the potential EUE-targeted gene in the therapy of ischemic stroke. DDIT4 expression was upregulated within cerebral brain samples of MCAO mice and OGD-triggered neuronal cells, and EUE could inhibit DDIT4 expression. The protective effect of EUE on neuronal cells could be partially reversed by overexpression of DDIT4. Moreover, EUE alleviated ferroptosis and improved neurological function in MCAO mice by suppressing DDIT4 expression and modulating the PI3K/Akt pathway. In conclusion, EUE exerts its neuroprotective effect against cerebral stroke by inhibiting DDIT4 expression and ferroptosis by regulating the PI3K/Akt pathway, and DDIT4 has been predicted to be an underlying therapeutic target for the treatment of ischemic stroke.</p>","PeriodicalId":49194,"journal":{"name":"Human Cell","volume":"38 6","pages":"166"},"PeriodicalIF":3.1,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145193585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}