Molecular and Cellular Biochemistry最新文献

{"title":"Bone marrow mesenchymal stem cells promote the recovery of stroke in rats with type 2 diabetes mellitus by inhibiting the activation of TLR4/NF-κB signaling pathway.","authors":"Fan Peng, Yanping Long, Taolin Zheng, Minghui Leng, Hui Deng","doi":"10.1007/s11010-025-05332-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05332-w","url":null,"abstract":"<p><p>Ischemic stroke is a major complication of type 2 diabetes mellitus (T2DM), significantly contributing to increased mortality in T2DM patients. Bone marrow mesenchymal stem cells (BMSCs), known for their multidirectional differentiation potential, have shown therapeutic potential in treating ischemic stroke associated with T2DM; however, the underlying mechanisms remain unclear. This study aimed to investigate the therapeutic effects and mechanisms of BMSCs in T2DM-related ischemic stroke. A T2DM rat model was established and subjected to transient middle cerebral artery occlusion (MCAO) to induce ischemic stroke. BMSCs were administered to evaluate their effects on body weight, blood glucose levels, modified neurological severity score (mNSS), infarct volume, and blood-brain barrier (BBB) integrity in T2DM-MCAO rats. RNA sequencing was performed on brain tissues from T2DM-MCAO rats before and after BMSCs treatment to identify differentially expressed genes (DEGs). Functional enrichment analysis, including Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, quantitative real-time PCR, and western blot, were conducted to explore the underlying mechanisms. The results demonstrated that T2DM-MCAO rats exhibited increased body weight, elevated blood glucose levels, higher mNSS scores, larger brain infarct volumes, and BBB disruption, all of which were partially ameliorated by BMSCs treatment. Furthermore, BMSCs downregulated the expression of TLR4 and reduced the protein levels of p65 and phosphorylated p65 (p-p65), which were upregulated in T2DM-MCAO rats. Overexpression of TLR4 partially reversed the beneficial effects of BMSCs on functional outcomes, infarct volume, and BBB integrity. In conclusion, this study demonstrates that BMSCs alleviate T2DM-related ischemic stroke by suppressing TLR4 expression and inhibiting the TLR4/NF-κB signaling pathway, suggesting a potential therapeutic target for T2DM-associated ischemic stroke.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275392","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 L-DOPA in neurological and neurodegenerative complications: a review.","authors":"Sudheendra Rao Kulkarni, Bothe Thokchom, Megha B Abbigeri, Santosh Mallikarjun Bhavi, Sapam Riches Singh, Nitish Metri, Ramesh Babu Yarajarla","doi":"10.1007/s11010-025-05324-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05324-w","url":null,"abstract":"<p><p>L-DOPA remains a cornerstone treatment for Parkinson's disease and is increasingly recognized for its role in various neurological and neurodegenerative disorders. As a direct precursor to dopamine, L-DOPA is synthesized from L-tyrosine through the action of tyrosine hydroxylase and is subsequently converted into dopamine via aromatic L-amino acid decarboxylase. Its ability to cross the blood-brain barrier (BBB) makes it a crucial therapeutic agent for restoring dopaminergic neurotransmission, thereby influencing motor function, cognition, and neuroprotection. Beyond Parkinson's, L-DOPA's therapeutic potential extends to neurodegenerative conditions such as Alzheimer's disease, Huntington's disease, multiple sclerosis, Lewy body dementia, and amyotrophic lateral sclerosis, where dopamine modulation plays a critical role. Furthermore, L-DOPA has demonstrated efficacy in neurological disorders including epilepsy, peripheral neuropathy, cerebrovascular diseases, and traumatic brain injury, suggesting broader neurobiological applications. However, long-term use is associated with challenges such as motor fluctuations, dyskinesias, and loss of therapeutic efficacy due to progressive neurodegeneration and alterations in dopaminergic pathways. Recent advancements in drug delivery systems, combination therapies, and nanotechnology, including plant-derived carbon dots, offer promising strategies to enhance L-DOPA's effectiveness while mitigating its limitations. This comprehensive review explores L-DOPA's synthesis, pharmacokinetics, mechanism of action, and its evolving role in neurological diseases, while highlighting ongoing challenges and future directions for optimizing its clinical application.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248705","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 randomized controlled trial on the impact of anesthetic agents on renal function in cardiac surgery with cardiopulmonary bypass.","authors":"Teng Fan, Zhili Zhao, Jun Liu, Wenke Ma, Jianmin Tian, Guifang Ma","doi":"10.1007/s11010-025-05326-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05326-8","url":null,"abstract":"<p><p>Acute kidney injury (AKI) is a frequent and severe problem following heart surgery, particularly in procedures involving cardiopulmonary bypass (CPB). This research investigates the Randomized Controlled Trial (RCT) on the impact of agents of anesthetic on renal function in patients receiving elective cardiac surgery and CPB, comparing propofol-based and volatile anesthetic-based regimens. A sum of 61 patients was randomly assigned into two regions: one receiving a propofol-based regimen and the other, a volatile anesthetic regimen, both combined with opioid analgesia. Renal function was assessed preoperatively and postoperatively at 24 and 48 h using serum creatinine and cystatin C levels. Perioperative inflammatory markers were deliberate to evaluate inflammation-mediated renal impairment multivariate logistic regression identified risk factors for AKI, and independent t-tests compared renal function parameters between regimens. Patients receiving propofol exhibited significantly lower rates of AKI ( <math><mrow><mtext>p</mtext> <mspace></mspace> <mo><</mo> <mn>0.05</mn></mrow> </math> ) and reduced inflammatory marker levels associated to the volatile anesthetic regimen. These results present that propofol anesthesia provides a protecting influence on renal function, likely due to its anti-inflammatory properties. The research emphasizes the necessity of choosing the right anesthetic for postoperative kidney outcomes by tailoring anesthetic regimens to mitigate AKI risk in high-risk populations. Propofol's protective role against AKI offers potential clinical value, particularly in cardiac surgeries requiring CPB. Further investigation with bigger cohorts and continued follow-up are necessary for verifying these findings and exploring their broader applicability in cardiac anesthesia.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144248704","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":"Agr2 in cancer and beyond: unraveling its role during protein synthesis, ER stress, and as a predictive biomarker.","authors":"Philip Salu, Katie M Reindl","doi":"10.1007/s11010-025-05318-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05318-8","url":null,"abstract":"<p><p>Protein folding is an essential component of protein biosynthesis, allowing for post-translational modifications that ensure proper protein structure and function to support cellular physiology. The presence of unfolded proteins triggers cellular mechanisms to either remove the unfolded proteins or reduce protein synthesis. However, the accumulation of improperly folded proteins may lead to diseases, including neurological disorders and cancers. Indeed, cancer cells have a dysregulated protein synthesis capacity that enables them to survive in higher proliferative and growth states. The anterior gradient 2 (Agr2) protein is often overexpressed in multiple cancers to support the need for increased protein synthesis resulting from uncontrolled cell proliferation. Agr2 acts like a protein disulfide isomerase (PDI), catalyzing the formation of disulfide bonds in native proteins. Its expression in cancers has been associated with increased cell proliferation, metastasis, and invasion. Conversely, the lack of Agr2 has been associated with ER stress (ERS) and the activation of the unfolded protein response (UPR) pathway to restore cellular protein homeostasis. Furthermore, Agr2 can be secreted into the extracellular environment and has been detected in human urine and serum, highlighting its potential use as a cancer biomarker. This review discusses Agr2 and its role in protein synthesis and ERS. We examine recent developments regarding its detection and use as a biomarker and delve into emerging therapeutic strategies focused on targeting Agr2.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225899","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":"Treatment with crocin attenuates cardiac metabolic disturbances and subsequent inflammation in streptozotocin-induced diabetes.","authors":"Dimitra Palioura, Konstantinos Feidantsis, Antigone Lazou","doi":"10.1007/s11010-025-05320-0","DOIUrl":"https://doi.org/10.1007/s11010-025-05320-0","url":null,"abstract":"<p><p>Diabetes mellitus (DM) is a metabolic disorder closely associated with cardiac dysfunction. Natural products are considered potential candidates for the management of DM. Crocin, a natural carotenoid derived from saffron, has been reported to possess several pharmacological properties, including cardioprotective effects. The aim of the present study was to investigate the beneficial effects of crocin on the metabolic derangement of the diabetic myocardium. Streptozotocin (STZ)-induced diabetic rats were treated with 10 mg/kg of crocin daily for two weeks. Oral administration of crocin normalized blood glucose, HbA1c, triglycerides, total cholesterol, LDL, and HDL levels. Notably, crocin reduced the elevated protein levels of cardiac PPARα and PPARδ-major transcriptional regulators of cardiac metabolism-back to normal. Consequently, the expression of the fatty acid (FA) transporter CD36 was downregulated, the activity of the FA oxidation enzyme 3-hydroxyacyl-CoA dehydrogenase (HOAD) was decreased, and intramyocardial triglyceride accumulation returned to physiological levels. Furthermore, crocin improved glucose uptake and metabolism in the diabetic myocardium, as evidenced by increased Akt phosphorylation, translocation of GLUT4 to the plasma membrane, enhanced activity of pyruvate kinase, and downregulation of pyruvate dehydrogenase kinase 4 (PDK4). Importantly, the stimulatory effect of crocin on Akt phosphorylation was also confirmed in isolated cardiac myocytes exposed to high glucose, further supporting its direct role in modulating glucose signaling pathways. Crocin treatment also reduced STZ-induced elevations in the levels of inflammatory cytokines-interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)-as well as the phosphorylation of IκBα, bringing them close to basal levels. Overall, these findings suggest that crocin activates Akt signaling and thereby alleviates diabetes-induced metabolic disturbances by restoring the balance between glucose and fatty acid utilization in the hearts of STZ-induced diabetic rats. Therefore, crocin supplementation may represent a promising approach for the development of natural compound-based adjunct therapies for diabetic cardiomyopathy.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216346","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":"Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway.","authors":"Qiuyan Wang, Yi Liang, Qingjuan Zuo, Lili He, Tingting Zhang, Zhongli Wang, Jianlong Zhai, Boce Cao, Sai Ma, Guorui Zhang, Fan Lu, Kaichuan He, Yan Wang, Yifang Guo","doi":"10.1007/s11010-025-05321-z","DOIUrl":"https://doi.org/10.1007/s11010-025-05321-z","url":null,"abstract":"<p><p>Hypertension and its complications seriously affect human health, bringing about long-term medical burdens, functional impairments and even death. This study explored the impact of Canagliflozin (CANA) on the blood vessels of salt-sensitive hypertension. Male Dahl salt-sensitive (Dahl SS) rats were fed with an 8% high-salt diet, and then intragastrically given CANA at a dose of 30 mg/kg/day or with a 0.5% hydroxypropyl methylcellulose solution for 12 weeks to induce hypertensive vascular damage and premature aging. Through vascular ultrasound detection, CANA improved the aortic stiffness and hemodynamics of high-salt-fed rats. Through vascular reactivity tests, CANA improved the carotid artery vasodilation. Hematoxylin and eosin (H&E), Sirius red, and senescence associated β-galactosidase staining were performed on the aorta, and CANA improved the fibrosis and aging of the aorta. CANA was found to reduce the expression of senescence associated secretory phenotype in the circulation that was induced by a high-salt diet. Additionally, it increased the expression of Sirtuin 6(SIRT6) in blood vessels and decreased the expression of Hypoxia-inducible factor 1α (HIF-1α) and its target genes. This study has demonstrated for the first time that CANA mitigates salt-induced aortic sclerosis and premature aging via the SIRT6/HIF-1α pathway.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199620","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":"PSAT1 promotes the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT.","authors":"Minshan Tang, Kai Song, Danning Xie, Xinyu Yuan, Yaxuan Wang, Zhiyang Li, Xiansheng Lu, Liang Guo, Xiaotong Zhu, Le Xiong, Wenqian Zhou, Jie Lin","doi":"10.1007/s11010-024-05194-8","DOIUrl":"10.1007/s11010-024-05194-8","url":null,"abstract":"<p><p>Colorectal cancer (CRC) ranks third for morbidity and second for mortality among all digestive malignant tumors worldwide, but its pathogenesis remains not entirely clear. Bioinformatic analyses were performed to find out important biomarkers for CRC. For validation, reverse transcription-quantitative PCR, western blotting, and immunohistochemistry were performed. Then, cell transfection, gain- and loss-of-function assays, immunofluorescence, cell line RNA-sequencing and analyses, and in vivo tumorigenesis assay were also performed to further explore the mechanism. We prioritized phosphoserine aminotransferase 1 (PSAT1) as an important biomarker in CRC. PSAT1 expression was gradually up-regulated as the CRC disease progresses and may relate to poor prognosis. PSAT1 promoted the malignant behaviors of CRC cells. Although PSAT1 is an enzyme essential to serine biosynthesis, an exogenous supplement of serine did not completely rescue the malignant behaviors in PSAT1-knockdown CRC cells. Interestingly, PSAT1 inhibited the Hippo tumor-suppressor pathway by promoting the nucleus-localization of YAP/TAZ and increasing the expression of ID1 in CRC cells. Furthermore, AMOT, a vascular-related molecule that molecularly interacts with YAP/TAZ, was up-regulated upon PSAT1 knockdown in CRC cells. Knocking down AMOT partially rescued the inhibition of proliferation and the reduced nuclear localization of YAP/TAZ caused by PSAT1 knockdown in CRC cells. Moreover, PSAT1 was closely related to vascular-related pathways, in which AMOT might act as a mediator. Finally, PSAT1 promoted CRC proliferation by negatively regulating AMOT in vivo. PSAT1 could enhance the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT, which is independent of the metabolic function of PSAT1.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3647-3668"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142910046","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":"Circular RNAs: key players in tumor immune evasion.","authors":"Mahla Sanati, Soudeh Ghafouri-Fard","doi":"10.1007/s11010-024-05186-8","DOIUrl":"10.1007/s11010-024-05186-8","url":null,"abstract":"<p><p>Immune responses against tumor antigens play a role in confining tumor growth. In response, cancer cells developed several mechanisms to bypass or defeat these anti-tumor immune responses-collectively referred to as \"tumor immune evasion\". Recent studies have shown that a group of non-coding RNAs, namely circRNAs affect several aspects of tumor immune evasion through regulation of activity of CD8 + T cells, regulatory T cells, natural killer cells, cytokine-induced killer cells or other immune cells. Understanding the role of circRNAs in this process facilitate design of novel therapies for enhancing the anti-tumor capacity of immune system. This review provides an outline of different roles of circRNAs in the tumor immune evasion.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3267-3295"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927613","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":"Selenium: 48-year journey of global clinical trials.","authors":"Yikun Wu, Jun Pei, Yuangao Xu, Fuxun Yu, Shuxiong Xu","doi":"10.1007/s11010-024-05202-x","DOIUrl":"10.1007/s11010-024-05202-x","url":null,"abstract":"<p><p>Selenium, an essential trace mineral for health, has seen a rise in clinical trials over the past nearly 5 decades. Our aim here is to provide a comprehensive and concise overview of selenium clinical trials from 1976 to 2023. Overall, the evolution of selenium clinical trials over 48 years has advanced through phases of emergence, prosperity, and either stability or transition. The USA plays pivotal roles in establishing large research clusters and fostering strong collaborative ties of selenium clinical trials. Low-selenium levels are noted in a higher proportion of selenium observational trials, while selenium intervention trials are delineated by nine key functional classifications. The emphasis in intervention trials is that selenium product development should be on conducting clinical trials in diseases with higher efficacy, such as those involving antioxidant and endocrine and metabolic disease. Moreover, inorganic forms such as sodium selenite and semi-organic forms like selenized yeast were recognized as primary sources of selenium, while nano-selenium has emerged as a new selenium source in clinical treatments. Selenium is mainly consumed through tablets and oral administration, with a recommended upper limit of 200 µg per day for managing most diseases. In addition, genes encoding selenoproteins or factors of relevance for selenium metabolism, inflammation, and immunity, which have a higher number of records in all trials, are poised to steer future investigations into functional mechanisms of selenium. We believe this review will offer fresh perspectives on selenium clinical trials and identify potential avenues for future selenium research.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3253-3265"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927616","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":"Metabolic reprogramming and signaling adaptations in anoikis resistance: mechanisms and therapeutic targets.","authors":"Chao He, Jie He","doi":"10.1007/s11010-024-05199-3","DOIUrl":"10.1007/s11010-024-05199-3","url":null,"abstract":"<p><p>Anoikis, a form of programmed cell death triggered by detachment from the extracellular matrix (ECM), maintains tissue homeostasis by removing mislocalized or detached cells. Cancer cells, however, have evolved multiple mechanisms to evade anoikis under conditions of ECM detachment, enabling survival and distant metastasis. Studies have identified differentially expressed proteins between suspended and adherent cancer cells, revealing that key metabolic and signaling pathways undergo significant alterations during the acquisition of anoikis resistance. This review explores the regulatory roles of epithelial-mesenchymal transition, cancer stem cell characteristics, metabolic reprogramming, and various signaling pathway alterations in promoting anoikis resistance. And the corresponding reagents and non-coding RNAs that target the aforementioned pathways are reviewed. By discussing the regulatory mechanisms that facilitate anoikis resistance in cancer cells, this review aims to shed light on potential strategies for inhibiting tumor progression and preventing metastasis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3315-3342"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008357","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}