Molecular and Cellular Biochemistry最新文献

{"title":"Roles of microRNAs in cardiorenal syndrome.","authors":"Yilin Ren, Hui Lin, Junnan Guo, Xiaole Su, Lihua Wang, Xi Qiao","doi":"10.1007/s11010-025-05253-8","DOIUrl":"10.1007/s11010-025-05253-8","url":null,"abstract":"<p><p>Cardiac and kidney diseases are intimately linked through numerous pathophysiological pathways, frequently exerting reciprocal influences on one another. This interconnection often culminates in heightened morbidity and mortality rates within the clinical spectrum of cardiorenal syndrome (CRS). CRS is categorized into five types based on the primary organ involved and the chronicity of the condition. Each type of CRS encompasses a complex array of pathophysiological mechanisms. In recent years, the field of microRNAs (miRNAs) has risen to prominence, playing a crucial role in the pathogenesis of a multitude of diseases. By uncovering novel therapeutic targets through the study of miRNAs that influence the expression of the CRS genes, the prognostic outcomes for patients could be significantly improved. This article provides a comprehensive review, examining the pathophysiological underpinnings of CRS, miRNAs alterations and their associated mechanisms in various forms of CRS, as well as the potential of miRNAs in precision medicine and the use of miRNAs for the diagnosis of the disease.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4069-4078"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710650","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":"Human dental follicle cell-derived conditioned media enhance periodontal regeneration by regulating the osteogenic differentiation and inflammation of periodontal ligament stem cells and macrophage polarization.","authors":"Yichen Gao, Xianyi He, Yuyao Deng, Xia Wang, Jie Shen, Wei Xu, Rui Cai, Xiaorong Lan, Junliang Chen, Yun He","doi":"10.1007/s11010-025-05260-9","DOIUrl":"10.1007/s11010-025-05260-9","url":null,"abstract":"<p><p>Dental follicle cells (DFCs) derived from the neural crest are promising seed cells for periodontal tissue engineering. This study aimed to investigate whether conditioned media (CM) from human DFCs could regenerate impaired periodontal tissue and the underlying mechanisms. hDFC-derived CM (hDFC-CM) were obtained via ultracentrifugation. In vitro, human periodontal ligament stem cells (hPDLSCs) were treated with hDFC-CM in normal and inflammatory microenvironments, and the cell proliferation, migration, and osteogenic potential were evaluated. We simulated the inflammatory environment with lipopolysaccharide and detected the expression of osteogenic and Wnt/β-catenin signaling pathway-related proteins. The effect of hDFC-CM on the inhibition of hPDLSC inflammation and macrophage polarization was examined. In vivo, the rat periodontitis model was treated with hDFC-CM. Tissue samples were collected after 4 weeks for micro-computed tomography and histological examination. The results of cell counting kit-8 and scratch experiments showed that hDFC-CM significantly enhanced the proliferation and migration capacities of hPDLSCs. hDFC-CM promoted the osteogenic differentiation of hPDLSCs by showing intense alkaline phosphatase and Alizarin Red staining and upregulated osteogenic protein and gene expression. Western blotting also verified that hDFC-CM promotes the osteogenic differentiation of hPDLSCs by regulating the Wnt/β-catenin pathway in an inflammatory environment. In addition, hDFC-CM inhibited hPDLSC inflammation and polarized macrophages from the M1 to M2 phenotype. In vivo, hDFC-CM effectively promoted periodontal tissue regeneration. hDFC-CM enhances periodontal regeneration by regulating the osteogenic differentiation and inflammation of periodontal ligament stem cells and macrophage polarization, which provided new biochemical cues for the treatment of periodontitis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4431-4448"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772453","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":"The role of LNK in mitigating hypertension: inhibition of vascular smooth muscle proliferation and JAK-STAT pathway.","authors":"Xinxin Han, Shuo Wei, Ali Ahmad, Yibo Cao, Caihong Zhao, Mengyang Yan, Jing Zhao, Xingmei Deng, Hongsu He, Zhihua Sun","doi":"10.1007/s11010-025-05237-8","DOIUrl":"10.1007/s11010-025-05237-8","url":null,"abstract":"<p><p>The lymphocyte adaptor protein LNK is predominantly found in endothelial and hematopoietic cells and is linked to cardiovascular and autoimmune diseases. LNK functions as a negative regulator of cytokine signaling and cell proliferation, but its impact on hypertensive vascular smooth muscle cells (HVSMC) remains unclear. This study aimed to explore the influence of LNK on HVSMC function. To achieve this, vascular smooth muscle cells (VSMCs) from rat thoracic aorta were isolated and identified using immunofluorescence. A hypertensive cell model was established by treatment with angiotensin-II, confirmed through the MTT method. Lentivirus was utilized to create stable silencing and overexpression of the LNK gene. Flow cytometry assessed VSMC cycle, proliferation, and migration levels, while ELISA measured IL-6, TNF-α, and IFN-γ expression levels. Real-time quantitative PCR and western blot were employed to analyze LNK, STAT3, JAK1, JAK2, JAK3 mRNA, and protein expression in rat VSMC. Immunofluorescence results indicated that most VSMCs expressed vimentin, with a proliferation rate of 48.5% in VSMCs treated with 100 nM angiotensin-II, confirming successful isolation and model construction of HVSMC. Compared to the control group, the angiotensin-II group exhibited increased HVSMCs in S and G2/M-phases of the cell cycle, decreased in G0/G1 phases, higher proliferation and migration capacity, and elevated inflammation levels. Additionally, JAK1, JAK2, and STAT3 signaling pathway-related mRNA and protein expression were significantly elevated. These effects were further intensified by the combined action of angiotensin-II and LNK silencing virus. Conversely, these effects were notably reduced when angiotensin-II was combined with the LNK overexpressing virus. These findings suggest that LNK mitigates the impact of hypertension and inflammation by inhibiting the proliferation, migration, and JAK-STAT signaling pathway of HVSMCs.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4107-4118"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143516177","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":"The role of NRF2 function and regulation in atherosclerosis: an update.","authors":"Siarhei A Dabravolski, Alexey V Churov, Dmitry F Beloyartsev, Tatiana I Kovyanova, Irina N Lyapina, Vasily N Sukhorukov, Alexander N Orekhov","doi":"10.1007/s11010-025-05233-y","DOIUrl":"10.1007/s11010-025-05233-y","url":null,"abstract":"<p><p>Atherosclerosis, a chronic inflammatory disease of the arteries, remains a leading cause of cardiovascular morbidity and mortality worldwide. This review examines the molecular mechanisms underlying NRF2 role in atherosclerosis, focusing on the recently defined intricate interplay between autophagy, the nuclear factor erythroid 2-related factor 2 (NRF2) pathway, microRNAs (miRNAs), and genes regulating NRF2 with atheroprotective effects. The NRF2/autophagy axis emerges as a critical regulator of cellular responses to oxidative stress and inflammation in atherosclerosis, with key players including Heat Shock Protein 90 (HSP90), Neuropeptide Y (NPY), and Glutaredoxin 2 (GLRX2). MiRNAs are identified as potent regulators of gene expression in atherosclerosis, impacting NRF2 signalling and disease susceptibility. Additionally, genes such as Prenyl diphosphate synthase subunit 2 (PDSS2), Sulfiredoxin1 (Srxn1), and Isocitrate dehydrogenase 1 (IDH1) are implicated in NRF2-dependent atheroprotective pathways. Future research directions include elucidating the complex interactions between these molecular pathways, evaluating novel therapeutic targets in preclinical and clinical settings, and addressing challenges related to drug delivery and patient heterogeneity. Despite limitations, this review underscores the potential for targeted interventions aimed at modulating NRF2/autophagy signalling and miRNA regulatory networks to mitigate atherosclerosis progression and improve cardiovascular outcomes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3935-3949"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536741","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":"Retraction Note: Molecular and biochemical evidence on the protective role of ellagic acid and silybin against oxidative stress-induced cellular aging.","authors":"Maryam Baeeri, Solmaz Mohammadi-Nejad, Mahban Rahimifard, Mona Navaei-Nigjeh, Shermineh Moeini-Nodeh, Reza Khorasani, Mohammad Abdollahi","doi":"10.1007/s11010-025-05266-3","DOIUrl":"10.1007/s11010-025-05266-3","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4531"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720599","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":"14-3-3ζ: an optimal housekeeping protein for western blot analysis in swine rotator cuff tendon studies.","authors":"Resmi Rajalekshmi, Vikrant Rai, Devendra K Agrawal","doi":"10.1007/s11010-025-05255-6","DOIUrl":"10.1007/s11010-025-05255-6","url":null,"abstract":"<p><p>Healthy biomechanics of the shoulder involving rotator cuff muscles and rotator cuff tendon (RCT) is pivotal for joint stability, yet co-morbid conditions like hyperlipidemia and hyperglycemia can lead to degenerative changes jeopardizing tendon integrity. A change in protein expression, the functional moiety for molecular events, may result in altered healing of RCT and prolonged morbidity. Expression and activity of proteins are critical while investigating the underlying molecular and cellular changes involved in tendinopathy. While investigating the changes in the protein expression of various inflammatory mediators, we observed that the Western Blot bands for commonly used housekeeping genes (GAPDH, β-actin, and α-tubulin) were not uniform in different tendon samples. Therefore, we investigated for an optimal housekeeping gene for Western blot analysis in swine RCT under normal and hyperlipidemic conditions, as this is essential for accurate normalization of protein expression. The study evaluated several housekeeping genes-GAPDH, beta-actin, alpha and beta-tubulin, Ubiquitin C, Cyclophilin A, TATA-box binding protein, and 14-3-3ζ-to ensure robust normalization across experimental setups. The results revealed that the protein expression of 14-3-3ζ was uniform in all samples, thereby validating its suitability as a stable housekeeping protein. The findings are important while studying the RCT pathology in a clinically relevant animal model, like swine, which mimics human RCT and provides translationally significant findings. Thus, the 14-3-3ζ protein will be an ideal housekeeping gene in the design of experiments utilizing musculoskeletal tissues.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4355-4363"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692573","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":"TCF7 functions as a prognostic biomarker in bladder cancer by strengthening EMT and stemness associated with TGF-β/SMAD3 signaling.","authors":"Congcong Zhang, Haiping Cai, Mengnan Ye, Le Wang, Weiwei Liu, Qun Huang, Xingsi Peng, Guanquan Mao, Qingling Zhang, Yan Mei","doi":"10.1007/s11010-025-05241-y","DOIUrl":"10.1007/s11010-025-05241-y","url":null,"abstract":"<p><p>Bladder cancer (BC) is one of the top ten most common tumors, with recurrence and metastasis being major causes of mortality among patients. A high recurrence rate is a hallmark of BC. Epithelial-mesenchymal transition (EMT) plays a role in the formation of cancer stem cells, tumor metastasis, and immune evasion. In our preliminary research, single-cell sequencing identified TCF7 as a gene associated with EMT. However, its biological function and transcriptional regulation mechanisms in BC remain unclear. This study aims to investigate TCF7's role and regulatory mechanisms in BC progression. TCF7 is a critical transcription factor promoting BC progression. High TCF7 expression in BC is significantly linked to poor patient prognosis. We uncovered a novel mechanism by which TCF7 drives EMT and stemness in BC through transcriptional regulation of TGFBR1, impacting the TGF-β/SMAD3 pathway. These findings enhance our understanding of BC progression and offer potential strategies for diagnosis, treatment, and prognosis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4135-4148"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536651","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":"LncRNA BDNF-AS binds to DNMT1 to suppress angiogenesis in glioma by promoting NEDD4L-mediated YAP1 ubiquitination.","authors":"Yongwen Deng, Jixin Feng, Jiangyang Li, Shuhui Gong, Shengli Sun","doi":"10.1007/s11010-025-05250-x","DOIUrl":"10.1007/s11010-025-05250-x","url":null,"abstract":"<p><p>Glioma, a highly aggressive brain tumor, is characterized by high mortality and frequent recurrence rates. Angiogenesis is a critical hallmark of glioma progression. However, the regulatory role and underlying mechanism of lncRNA brain-derived neurotrophic factor-antisense (BDNF-AS) in glioma angiogenesis remain poorly understood and warrant further investigation. Malignant characteristics of glioma cells were evaluated using CCK-8, colony formation, scratch, transwell, flow cytometry, and tube formation assays. The expression levels of genes and proteins were detected by RT-qPCR, western blot, and IHC assays. The methylation level of NEDD4-like E3 ubiquitin protein ligase (NEDD4L) was determined using MSP. The interactions among molecules were validated using RIP, ChIP, and Co-IP. Our study revealed significantly downregulated BDNF-AS expression in glioma cells. BDNF-AS overexpression markedly attenuated the malignant characteristics of glioma cells, as evidenced by decreased viability, proliferation, migration, invasion, and angiogenesis, along with increased apoptosis. These tumor-suppressive effects were significantly abrogated by NEDD4L knockdown. Mechanistically, BDNF-AS could interact with DNA methyltransferase 1 (DNMT1) expression, leading to reduced NEDD4L promoter methylation and upregulation of NEDD4L expression. Additionally, NEDD4L-mediated promotion of YAP1 ubiquitination to decline YAP1 and VEGFA expression. Finally, BDNF-AS exerted potent anti-tumor effects by mediating NEDD4L/YAP1/VEGFA axis, as demonstrated by suppressed tumor growth in glioma-bearing mice and attenuated malignant features in glioma cells. BDNF-AS suppressed cell viability, proliferation, migration, and invasion, and promoted cell apoptosis of glioma cells, attenuated angiogenesis of human umbilical vein endothelial cells (HUVECs), and tumor growth via regulating NEDD4L/YAP1/VEGFA axis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4325-4341"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143677129","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":"TOR1 AIP1 interacts with p53 to enhance cell cycle dysregulation in prostate cancer progression.","authors":"Zhaofeng Li, Xueyu Li, Han Yang, Meixiang Huang, Zhu Liu, Zongliang Zhang, Kai Zhao, Xinbao Yin, Guanqun Zhu, Yulian Zhang, Zhenlin Wang, Qinglei Wang, Zaiqing Jiang, Suofei Zhang, Tianzhen He, Ke Wang","doi":"10.1007/s11010-025-05276-1","DOIUrl":"10.1007/s11010-025-05276-1","url":null,"abstract":"<p><p>The cell cycle mechanism is an integration point where information is sent through an upstream signaling network, making it a potential target for cancer diagnosis and treatment. The LAP1 protein, encoded by the Tor1aip1 gene, is required to maintain the shape of the nuclear envelope and the progression of the cell cycle. The aim of this study was to determine the role of Tor1aip1 gene in PRAD development and its mechanism. We analyzed the expression and survival data of TOR1 AIP1 in PRAD patients in the TCGA database and verified the low expression of TOR1 AIP1 in prostate cancer by qPCR, western blot and immunohistology, which was correlated with the tumor stage and survival prognosis of PRAD. In addition, lentiviral vectors were used to mediate the up-regulation or down-regulation of TOR1 AIP1 expression in prostate cancer cells, and the effects of TOR1 AIP1 on tumor proliferation and related signaling pathways were investigated by cell counting kit- 8, colony formation assay, transwell assay, western blot, and flow cytometry. As a result, we found that TOR1 AIP1 enhances protein stability of p53 by directly interacting with p53, consequently inhibited tumor proliferation and invasion by inducing the cell cycle to be arrested in the S phase. Therefore, TOR1 AIP1 represents a promising therapeutic target in PRAD due to its ability to stabilize p53 and enhance its tumor-suppressive functions. Future studies should focus on elucidating its mechanisms, developing targeted therapies, and exploring its clinical potential in combination with existing treatments. By advancing our understanding of TOR1 AIP1, we may unlock new strategies for improving outcomes in PRAD patients.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"4483-4497"},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811776","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":"Hypoxia-induced histone lactylation promotes pulmonary arterial smooth muscle cells proliferation in pulmonary hypertension.","authors":"Ai Chen, Zhihai Chen, Bangbang Huang, Guili Lian, Li Luo, Liangdi Xie","doi":"10.1007/s11010-025-05342-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05342-8","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling and excessive proliferation of pulmonary artery smooth muscle cells (PASMCs). Glycolysis plays a crucial role in PH pathogenesis, but the epigenetic mechanisms linking glycolysis to PASMCs proliferation remain unclear. Histone lactylation, a novel post-translational modification derived from glycolytic lactate, may regulate PASMCs proliferation. Primary rat PASMCs were cultured under hypoxia and treated with sodium L-lactate (NaLa) to assess glycolytic activity and histone lactylation. RNA sequencing, RT-qPCR, and Western blotting identified differentially expressed genes (DEGs), while ChIP-qPCR evaluated histone lactylation enrichment at gene promoters. In vivo, a hypoxia-induced PH rat model was used to examine the effect of glycolysis inhibition using oxamate. Mendelian randomization (MR) analysis assessed the causal relationship between placental growth factor (PGF) and PH. Hypoxia and NaLa treatment significantly increased glycolytic activity, lactate production, and histone lactylation, promoting PASMCs proliferation. Transcriptomic analysis identified 157 DEGs, with five key genes (Gbe1, Pgf, Mt2A, Ythdf2 and Gys1) upregulated in response to histone lactylation. ChIP-qPCR confirmed H3K18la enrichment at their promoters. Glycolysis inhibition with oxamate effectively reduced histone lactylation, PASMCs proliferation, and vascular remodeling in hypoxic PH rats. MR analysis identified PGF as a causal factor contributing to PH risk, suggesting a potential therapeutic target. This study reveals that glycolysis-induced histone lactylation drives PASMCs proliferation and vascular remodeling in PH. Targeting lactate metabolism and histone lactylation may provide a novel therapeutic approach.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528917","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}