Molecular and Cellular Biochemistry最新文献

{"title":"The highs and lows of monoamine oxidase as molecular target in cancer: an updated review.","authors":"Iasmina M Hâncu, Silvia Giuchici, Adina V Furdui-Lința, Bogdan Lolescu, Adrian Sturza, Danina M Muntean, Maria D Dănilă, Rodica Lighezan","doi":"10.1007/s11010-024-05192-w","DOIUrl":"10.1007/s11010-024-05192-w","url":null,"abstract":"<p><p>The global burden of cancer as a major cause of death and invalidity has been constantly increasing in the past decades. Monoamine oxidases (MAO) with two isoforms, MAO-A and MAO-B, are mammalian mitochondrial enzymes responsible for the oxidative deamination of neurotransmitters and amines in the central nervous system and peripheral tissues with the constant generation of hydrogen peroxide as the main deleterious ancillary product. However, given the complexity of cancer biology, MAO involvement in tumorigenesis is multifaceted with different tumors displaying either an increased or decreased MAO profile. MAO inhibitors are currently approved for the treatment of neurodegenerative diseases (mainly, Parkinson's disease) and as secondary/adjunctive therapeutic options for the treatment of major depression. Herein, we review the literature characterizing MAO's involvement and the putative role of MAO inhibitors in several malignancies, and also provide perspectives regarding the potential biomarker role that MAO could play in the future in oncology.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3225-3252"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876885","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":"Crocin and gallic acid attenuate ethanol-induced mitochondrial dysfunction via suppression of ROS formation and inhibition of mitochondrial swelling in pancreatic mitochondria.","authors":"Ahmad Salimi, Saleh Khezri, Mojtaba Amani, Niknaz Badrinezhad, Sahar Hosseiny, Reza Saadati","doi":"10.1007/s11010-024-05180-0","DOIUrl":"10.1007/s11010-024-05180-0","url":null,"abstract":"<p><p>Chronic/heavy exposure with ethanol is associated with risk of type 2 diabetes, due to β-cells dysfunction. It has been reported that ethanol can induce oxidative stress directly or indirectly by involvement of mitochondria. We aimed to explore the protective effects of the crocin/gallic acid/L-alliin as natural antioxidants separately on ethanol-induced mitochondrial damage. Intact mitochondria are isolated from pancreas by differential centrifugation and directly treated with toxic concentrations of ethanol (8% v/v) in the presence of different concentrations crocin/gallic acid/L-alliin (100, 500, and 1000 µM). Biomarkers of mitochondrial toxicity including the succinate dehydrogenases (SDH) activity, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), mitochondrial swelling, lipid peroxidation, and glutathione content were assessed. The results showed that 8% v/v ethanol-treated rat pancreas-isolated mitochondria for 1 h resulted in a significant decrease of SDH activity to 81.34 ± 3.48%, a significant increase of ROS formation, MDA content, mitochondrial swelling, and collapse of MMP. Among three tested natural compounds, treatment with crocin and gallic acid significantly reversed the changes of the above indicators and resulted in the increase of SDH activity, improvement of MMP collapse and mitochondrial swelling, and reduction of ROS formation and oxidative stress in pancreas-isolated mitochondria. This study demonstrated that crocin and gallic acid had direct protective effects on the mitochondrial damages induced by ethanol in pancreas-isolated mitochondria, and these natural compounds could be developed as mitochondrial protective agents in the prevention of pancreatic β-cells and diabetogenic effect of ethanol.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3669-3682"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927615","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":"GNA15 induces drug resistance in B cell acute lymphoblastic leukemia by promoting fatty acid oxidation via activation of the AMPK pathway.","authors":"Jie Luo, Shirui Pan, Jing Luo, Lan Wang, Jiaxiu Yin, Haiqiu Zhao, Rong Su, Mingyan Liao, Lin Liu, Jiamin Zhang","doi":"10.1007/s11010-024-05198-4","DOIUrl":"10.1007/s11010-024-05198-4","url":null,"abstract":"<p><p>The prognosis of B cell acute lymphoblastic leukemia (B-ALL) is poor, primarily due to drug resistance and relapse. Ga15, encoded by GNA15, belongs to the G protein family, with G protein-coupled receptors playing a crucial role in multiple biological process. GNA15 has been reported to be involved in various malignancies; however, its potential role in B-ALL remain unknown. In this study, high expression of GNA15 in B-ALL was observed in multiple databases. We further confirmed an increased transcriptional level of GNA15 in newly diagnosed B-ALL patients which was closely correlated with relapse. We showed that GNA15 promoted cell growth, inhibited apoptosis and enhanced drug resistance in leukemia cell lines. Metabolomics analysis revealed a significant enrichment of fatty acid oxidation (FAO) according to the GNA15 expression. We further confirmed that GNA15 could enhance FAO process as evidenced by the upregulation of key molecules involved in FAO including carnitine palmitoyl transferase1 (CPT1), CPT2 and CD36. And inhibition of FAO using etomoxir partially reversed the drug resistance caused by high expression of GNA15. Mechanism study showed that GNA15 promoted FAO by up-regulation of AMPK phosphorylation thus leading to survival advantage in leukemia cells. In conclusion, we observed elevated GNA15 transcript levels in B-ALL, which were associated with relapse. GNA15 could induce drug resistance though activation of the AMPK/FAO axis in leukemia cell lines. Targeting GNA15 and FAO may represent potential therapeutic strategy for improving the prognosis of B-ALL.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3719-3733"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142984068","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":"The role of α-tocopherol in the prevention and treatment of Alzheimer's disease.","authors":"Michał Pelczarski, Szymon Wolaniuk, Monika Zaborska, Jakub Sadowski, Anna Sztangreciak-Lehun, Rafał Jakub Bułdak","doi":"10.1007/s11010-025-05214-1","DOIUrl":"10.1007/s11010-025-05214-1","url":null,"abstract":"<p><p>Scientific reports from various areas of the world indicate the potential role of tocopherols (vitamin E) in particular α-tocopherol in the prevention and therapy of Alzheimer's disease. The current phenomenon is related to the growing global awareness of eating habits and is also determined by the need to develop the prevention, management and therapy of Alzheimer's disease. This article is a review of current research on the action of the active form of vitamin E-α-tocopherol and its impact on the development and course of Alzheimer's disease. Additionally, to contrast this information, selected primary research on this topic was included. The aim of this article is to analyze and summarize the available scientific information on the effects of the active form of vitamin E, α-tocopherol, on the development and course of Alzheimer's disease. In the structure of the review, particular attention was paid to the analysis of the pathophysiological processes of the disease and the biochemical features of the action of α-tocopherol. To discuss the relationship between the effect of α-tocopherol and the occurrence of Alzheimer's disease, a literature review was conducted using the following databases: PubMed, Google Scholar, and Elsevier. During the search process, the following keywords were used: \"tocopherols\", \"vitamin E\", \"α-tocopherol\", \"Alzheimer's disease\" in various combinations. The process was conducted in accordance with the adopted search strategy taking into account the inclusion and exclusion criteria. Alzheimer's disease (AD) is the most common, irreversible neurodegenerative disease, so many scientists are actively looking for substances and/or strategies to prevent its development and to slow down its course in patients. Alpha-tocopherols (ATF) are a factor that inhibits the pathophysiological processes associated with the development of AD by reducing the formation of atherogenic amyloid B (AB). Additionally, this type of tocopherols has antioxidant and anti-inflammatory properties and has a positive effect on the metabolic functioning of mitochondria. It has been shown that a higher intake of α-tocopherol (ATF) was associated with a reduced risk of developing dementia and the occurrence of mild types of cognitive impairment (MCI). Various sources indicate an insufficient supply of ATF in the diet. ATF supplementation may potentially help to slow down the course of Alzheimer's disease, which is why this substance may be popularized in the treatment of this disease in the future. However, there is a need for further research on this issue.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3385-3398"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008364","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 sirtuins in the regulation of reactive oxygen species in myocardial ischemia/reperfusion injury.","authors":"Zheng Wang, Xiaopeng Zhao, Mingjing Lu, Naiyu Wang, Shu Xu, Dongyu Min, Lijie Wang","doi":"10.1007/s11010-024-05204-9","DOIUrl":"10.1007/s11010-024-05204-9","url":null,"abstract":"<p><p>Myocardial ischemia/reperfusion (I/R) injury has high morbidity and mortality rates, posing a significant burden on society. There is an urgent need to understand its pathogenesis and develop effective treatments. Reactive oxygen species (ROS) are crucial for the development of myocardial I/R injury, and inhibiting ROS overproduction is one of the most critical ways to delay myocardial I/R injury. Sirtuins are a group of nicotinic adenine dinucleotide ( +)-dependent histone deacetylases whose members can regulate ROS by modulating various biological processes. Numerous studies have shown that Sirtuins play an essential role in the progression of myocardial I/R injury by regulating ROS. This study focuses on the relationship between myocardial I/R injury and ROS, Sirtuins and ROS, discusses the role of Sirtuins in regulating ROS in myocardial I/R, and summarizes the therapeutic modalities aimed at targeting Sirtuins to modulate ROS in myocardial I/R injury, thereby guiding future research endeavors.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3501-3520"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370878","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":"Novel insights into the central protective role of ACE2 in diabetic cardiomyopathy: from underlying signaling pathways to therapeutic perspectives.","authors":"Xinyi Li, Shunlin Qu","doi":"10.1007/s11010-024-05196-6","DOIUrl":"10.1007/s11010-024-05196-6","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DCM) is a cardiac complication specific to individuals with diabetes. It is defined as abnormalities of myocardial structure and function in diabetic patients who do not exhibit any obvious coronary artery disease, hypertensive heart disease, valvular heart disease, or inherited cardiomyopathy. A significant cardiovascular protective factor identified recently is angiotensin-converting enzyme 2 (ACE2), which is a rising star in the renin angiotensin system (RAS) and is responsible for the onset and progression of DCM. Nonetheless, there is not a comprehensive review outlining ACE2's effect on DCM. From the perspective of the pathogenesis of DCM, this review summarizes the myocardial protective role of ACE2 in the aspects of alleviating myocardial structure and dysfunction, correcting energy metabolism disorders, and restoring vascular function. Concurrently, we propose the connections between ACE2 and underlying signaling pathways, including ADAM17, Apelin/APJ, and Nrf2. Additionally, we highlight ACE2-related pharmaceutical treatment options and clinical application prospects for preventing and managing DCM. Further and underlying research is extensively required to completely comprehend the principal pathophysiological mechanism of DCM and the distinctive function of ACE2, switching experimental findings into clinical practice and identifying efficient therapeutic approaches.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3535-3551"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382939","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":"Olaparib reverses prostate cancer resistance to Rapamycin by promoting macrophage polarization towards the M1 phenotype.","authors":"Kai Ye, Gang Shi, Jian Xu, Kunyan Qiao, Qinghai Dai, Zhixiao Huo, Yu Cao, Wei Liu, Yue Hu, Lihua Yan, Yu Zhu, Ping Li, Rui Su, Liang Xu, Yuqiang Mi","doi":"10.1007/s11010-025-05231-0","DOIUrl":"10.1007/s11010-025-05231-0","url":null,"abstract":"<p><p>Prostate cancer (PCa) is the most common non-cutaneous malignancy and the second leading cause of cancer-related death in men. Despite its prevalence, treatment outcomes are often unsatisfactory, necessitating the search for more effective therapeutic approaches. mTOR inhibitor Rapamycin (RAPA) has shown promise in managing PCa, but the emergence of resistance often undermines its long-term effectiveness. Recent studies suggest that poly ADP-ribose polymerase (PARP) inhibitor Olaparib (OLP) may overcome drug resistance in various tumor types. This study aims to assess the efficacy of OLP in treating RAPA-resistant PCa, with a specific focus on elucidating its underlying molecular mechanisms. This study utilized drug exposure and concentration escalation experiments to establish human RAPA-resistant PCa cell line (PC-3R) based on the human PCa cell line (PC-3). PC-3R cell lines were screened through a cloning assay. The efficacy of OLP in RAPA-resistant PCa, as well as its regulatory impact on tumor-associated macrophages (TAMs), was evaluated through a combination of real-time PCR, ELISA, immunohistochemistry, and fluorescence experiments. This study unveiled that the combination of OLP and RAPA effectively suppressed the proliferation, stemness, invasion, angiogenesis, apoptosis resistance, and anti-oxidative stress capacity of RAPA-resistant PCa. Additionally, it demonstrated the capacity of OLP to regulate macrophage polarization within the tumor microenvironment and reverse drug resistance to RAPA in PCa. The findings of this study lay a theoretical foundation for the potential utilization of OLP in the treatment of RAPA-resistant PCa, offering substantial academic significance and promising application prospects.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3907-3921"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143472698","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":"Autophagy and the peroxisome proliferator-activated receptor signaling pathway: A molecular ballet in lipid metabolism and homeostasis.","authors":"Pouria Kiani, Elaheh Sadat Khodadadi, Ali Nikdasti, Sahar Yarahmadi, Mobina Gheibi, Zeynab Yousefi, Sajad Ehtiati, Sheida Yahyazadeh, Sayed Mohammad Shafiee, Motahareh Taghizadeh, Somayeh Igder, Seyyed Hossein Khatami, Saeed Karima, Omid Vakili, Morteza Pourfarzam","doi":"10.1007/s11010-025-05207-0","DOIUrl":"10.1007/s11010-025-05207-0","url":null,"abstract":"<p><p>Lipids, which are indispensable for cellular architecture and energy storage, predominantly consist of triglycerides (TGs), phospholipids, cholesterol, and their derivatives. These hydrophobic entities are housed within dynamic lipid droplets (LDs), which expand and contract in response to nutrient availability. Historically perceived as a cellular waste disposal mechanism, autophagy has now been recognized as a crucial regulator of metabolism. Within this framework, lipophagy, the selective degradation of LDs, plays a fundamental role in maintaining lipid homeostasis. Dysregulated lipid metabolism and autophagy are frequently associated with metabolic disorders such as obesity and atherosclerosis. In this context, peroxisome proliferator-activated receptors (PPARs), particularly PPAR-γ, serve as intracellular lipid sensors and master regulators of gene expression. Their regulatory influence extends to both autophagy and lipid metabolism, indicating a complex interplay between these processes. This review explores the hypothesis that PPARs may directly modulate autophagy within the realm of lipid metabolism, thereby contributing to the pathogenesis of metabolic diseases. By elucidating the underlying molecular mechanisms, we aim to provide a comprehensive understanding of the intricate regulatory network that connects PPARs, autophagy, and lipid homeostasis. The crosstalk between PPARs and other signaling pathways underscores the complexity of their regulatory functions and the potential for therapeutic interventions targeting these pathways. The intricate relationships among PPARs, autophagy, and lipid metabolism represent a pivotal area of research with significant implications for understanding and treating metabolic disorders.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3477-3499"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075263","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":"Ferroptosis in TNBC: interplay with tumor-infiltrating immune cells and therapeutic implications.","authors":"Lihong Hu, Jiejie Hu, Chengdong Qin, Siyuan Liu, Yang Yu","doi":"10.1007/s11010-025-05305-z","DOIUrl":"https://doi.org/10.1007/s11010-025-05305-z","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options and a poor prognosis. Immunotherapy has emerged as a promising approach for TNBC, with tumor-infiltrating immune cells (TICs) in the tumor microenvironment (TME) serving as a critical cellular basis for its efficacy. However, the success of immunotherapy in TNBC is often limited due to the immunosuppressive nature of the TME and the heterogeneity of TNBC. Ferroptosis, a form of iron-dependent programmed cell death regulated by metabolic networks including iron, glutathione (GSH), and lipid metabolism, has shown potential to enhance anti-tumor immunity. Recent studies have demonstrated that ferroptosis can modulate immune responses by promoting the infiltration and activation of TICs, thereby improving the outcomes of immunotherapy. However, ferroptosis in immunosuppressive cells such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) can trigger an \"immunosuppressive wave,\" affecting other immune cells in the tumor immune microenvironment. This demonstrates the dual role of ferroptosis in TNBC therapy, emphasizing the need for a nuanced understanding of its effects on different immune cells and tumor cells. Herein, we further elaborate the role of ferroptosis in TNBC cells and its interactions with tumor-infiltrating immune cells (TICs) within the TME.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173922","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":"Nuclear-localized metabolic enzymes: emerging key players in tumor epigenetic regulation.","authors":"Limei Chen, Zhihui Wu, Weixi Yuan, Nan Chen, Peina Lin, Senyi Liao, Guopeng Xie","doi":"10.1007/s11010-025-05316-w","DOIUrl":"https://doi.org/10.1007/s11010-025-05316-w","url":null,"abstract":"<p><p>Advancements in tumor research have highlighted the potential of epigenetic therapies as a targeted approach to cancer treatment. However, the application of these therapies has faced challenges due to the issue of substrate availability since the discovery of epigenetic modifications. Interestingly, metabolic changes are closely associated with epigenetic changes, and notably, certain metabolic enzymes exhibit nuclear localization within epigenetically active cellular contexts. This suggests that nuclear localization of metabolic enzymes may provide a mechanistic foundation for addressing substrate availability issues in epigenetic regulation. To date, there has been limited progress in synthesizing this information systematically. In this study, we provide an overview of the interplay between metabolic enzymes and epigenetic mechanisms, highlighting their critical roles. Subsequently, we summarize recent advances regarding the nuclear localization of metabolic enzymes, shedding light on their emerging roles in epigenetic regulation and oncogenesis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144160440","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}