Molecular and Cellular Biochemistry最新文献

{"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}

{"title":"Exploring ferroptosis and miRNAs: implications for cancer modulation and therapy.","authors":"Mobarakeh Ajam-Hosseini, Sadegh Babashah","doi":"10.1007/s11010-024-05169-9","DOIUrl":"10.1007/s11010-024-05169-9","url":null,"abstract":"<p><p>Ferroptosis is a novel, iron-dependent form of non-apoptotic cell death characterized by the accumulation of lipid reactive oxygen species (ROS) and mitochondrial shrinkage. It is closely associated with the onset and progression of various diseases, especially cancer, at all stages, making it a key focus of research for developing therapeutic strategies. Numerous studies have explored the role of microRNAs (miRNAs) in regulating ferroptosis by modulating the expression of critical genes involved in iron metabolism and lipid peroxidation. Due to their diversity, unique properties, and dynamic expression patterns in diseases, exosomal miRNAs are emerging as promising biomarkers. Exosomes act as biological messengers, delivering miRNAs to target cells through specific internalization, thus influencing the ferroptosis response in recipient cells. This review summarizes the roles of miRNAs, with particular focus on exosomal miRNAs, in ferroptosis and their implications for cancer pathology. By examining the molecular mechanisms of miRNAs, we aim to provide valuable insights into potential therapeutic approaches.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3455-3476"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047154","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":"Irisin: muscle's novel player in endoplasmic reticulum stress and disease.","authors":"Joel Rimson Pinto, K Deepika Bhat, Bipasha Bose, P Sudheer Shenoy","doi":"10.1007/s11010-025-05225-y","DOIUrl":"10.1007/s11010-025-05225-y","url":null,"abstract":"<p><p>Irisin, an exercise-induced myokine, exhibits elevated levels during physical activity, yet its role in modulating the unfolded protein response (UPR) remains poorly understood. This comprehensive review pioneers an in-depth examination of irisin-mediated endoplasmic reticulum (ER) stress mitigation across various diseases. We provide a nuanced characterization of irisin's molecular profile, biological activity, and significance as a skeletal muscle-derived cytokine analogue. Our discussion elucidates the complex interplay between exercise, irisin signalling, and metabolic outcomes, highlighting key molecular interactions driving salutary effects. Moreover, we delineate the UPR's role as a critical ER stress countermeasure and underscore irisin's pivotal function in alleviating this stress, revealing potential therapeutic avenues for disease management. Exercise-induced release of irisin ameliorates ER stress through AMPK phosphorylation during various diseases (Icon image source: www.flaticon.com ).</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3605-3619"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143472694","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":"Epigallocatechin 3-gallate-induced neuroprotection in neurodegenerative diseases: molecular mechanisms and clinical insights.","authors":"Md Rezaul Islam, Abdur Rauf, Sumiya Akter, Happy Akter, Md Ibrahim Khalil Al-Imran, Samiul Islam, Meherun Nessa, Chaity Jahan Shompa, Md Nabil Rihan Shuvo, Imtiaz Khan, Waleed Al Abdulmonem, Abdullah S M Aljohani, Muhammad Imran, Marcello Iriti","doi":"10.1007/s11010-025-05211-4","DOIUrl":"10.1007/s11010-025-05211-4","url":null,"abstract":"<p><p>Neurodegenerative diseases (NDs) are caused by progressive neuronal death and cognitive decline. Epigallocatechin 3-gallate (EGCG) is a polyphenolic molecule in green tea as a neuroprotective agent. This review evaluates the therapeutic effects of EGCG and explores the molecular mechanisms that show its neuroprotective properties. EGCG protects neurons in several ways, such as by lowering oxidative stress, stopping Aβ from aggregation together, changing cell signaling pathways, and decreasing inflammation. Furthermore, it promotes autophagy and improves mitochondrial activity, supporting neuronal survival. Clinical studies have demonstrated that EGCG supplementation can reduce neurodegenerative biomarkers and enhance cognitive function. This review provides insights into the molecular mechanisms and therapeutic potential of EGCG in treating various NDs. EGCG reduces oxidative stress by scavenging free radicals and enhancing antioxidant enzyme activity, aiding neuronal defense. It also protects neurons and improves cognitive abilities by inhibiting the toxicity and aggregation of Aβ peptides. It changes important cell signaling pathways like Nrf2, PI3K/Akt, and MAPK, which are necessary for cell survival, cell death, and inflammation. Additionally, it has strong anti-inflammatory properties because it inhibits microglial activation and downregulates pro-inflammatory cytokines. It improves mitochondrial function by reducing oxidative stress, increasing ATP synthesis, and promoting mitochondrial biogenesis, which promotes neurons' survival and energy metabolism. In addition, it also triggers autophagy, a cellular process that breaks down and recycles damaged proteins and organelles, eliminating neurotoxic aggregates and maintaining cellular homeostasis. Moreover, it holds significant promise as an ND treatment, but future research should focus on increasing bioavailability and understanding its long-term clinical effects. Future studies should focus on improving EGCG delivery and understanding its long-term effects in therapeutic settings. It can potentially be a therapeutic agent for managing NDs, indicating a need for further research.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3363-3383"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008352","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":"Angiogenic Markers in Gestational Diabetes and their Association with Placental Dimensions.","authors":"Shweta Madiwale, Vaishali Kasture, Deepali Sundrani, G V Krishnaveni, Sanjay Gupte, Sadhana Joshi","doi":"10.1007/s11010-024-05189-5","DOIUrl":"10.1007/s11010-024-05189-5","url":null,"abstract":"<p><p>GDM is an increasing global concern, with its etiology not fully understood, though altered placental function is likely to play a role. Placental angiogenesis, essential for sufficient blood flow and nutrient exchange between mother and fetus, may be affected by GDM. However, the role of angiogenic markers in GDM remains unclear. This study aims to investigate angiogenic markers from early pregnancy till delivery and their relationship with placental dimensions. This study is a part of a longitudinal study, where a total of 1154 women were recruited, out of which 167 women developed GDM (15.2%). The current study includes a total of 130 women randomly selected (65 GDM and 65 Non-GDM women). Plasma and placental levels of angiogenic markers such as VEGF, PLGF and sFlt-1/Flt-1 were estimated. Placental dimensions and birth outcomes were recorded, and associations between angiogenic markers and these parameters were examined. sFlt-1 (p < 0.05) levels were higher at V1 (11-14 weeks) in GDM women as compared to Non-GDM women. Placental PLGF (p < 0.01) and Flt-1 (p < 0.05) levels were lower in the GDM group. PLGF and Flt-1 were negatively associated with placental dimensions such as major axis, minor axis and breadth of the placenta. This study reveals altered expression of placental angiogenic markers in women with GDM, potentially affecting placental development and function. Negative correlations between these markers and placental dimensions suggest their influence on pregnancy outcomes in GDM.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3637-3646"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142896167","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":"METTL3: a multifunctional regulator in diseases.","authors":"Na Li, Xiang Wei, Jian Dai, Jinfeng Yang, Sizheng Xiong","doi":"10.1007/s11010-025-05208-z","DOIUrl":"10.1007/s11010-025-05208-z","url":null,"abstract":"<p><p>N6-methyladenosine (m⁶A) methylation is the most prevalent and abundant internal modification of mRNAs and is catalyzed by the methyltransferase complex. Methyltransferase-like 3 (METTL3), the best-known m⁶A methyltransferase, has been confirmed to function as a multifunctional regulator in the reversible epitranscriptome modulation of m⁶A modification according to follow-up studies. Accumulating evidence in recent years has shown that METTL3 can regulate a variety of functional genes, that aberrant expression of METTL3 is usually associated with many pathological conditions, and that its expression regulatory mechanism is related mainly to its methyltransferase activity or mRNA posttranslational modification. In this review, we discuss the regulatory functions of METTL3 in various diseases, including metabolic diseases, cardiovascular diseases, and cancer. We focus mainly on recent progress in identifying the downstream target genes of METTL3 and its underlying molecular mechanisms and regulators in the above systems. Studies have revealed that the use of METTL3 as a therapeutic target and a new diagnostic biomarker has broad prospects. We hope that this review can serve as a reference for further studies.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3429-3454"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033702","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":"Galium verum L. extract mitigates cardiovascular events in psoriasis rats.","authors":"Milena Corbic, Vladimir Jakovljevic, Marina Nikolic, Nevena Jeremic, Jovana Bradic, Jovana Novakovic, Aleksandar Kocovic, Maja Savic, Vanja Tadic, Ana Zugic, Milos Krivokapic, Branislava Daskalovic, Katarina Mihajlovic, Jasmina Sretenovic","doi":"10.1007/s11010-025-05215-0","DOIUrl":"10.1007/s11010-025-05215-0","url":null,"abstract":"<p><p>Psoriasis has been considered a systemic immune-mediated disease that can affect function of the heart. However, certain herbal therapy approaches may nullify side effects of psoriasis on the heart. The aim of this study was to investigate the cardioprotective effects of Galium verum extract administration of the heart of psoriatic rats. The study included 24 Wistar albino male rats, divided into 4 groups: control (CTRL), G.verum (GV), psoriasis (PSORI), and psoriasis with G.verum (PSORI + GV). Seven-day topical application of 5% imiquimod cream was used for induction of psoriasis. After induction, animals were received 125 mg/kg G.verum extract for 4 weeks. Isolated hearts were perfused on the Langendorff apparatus and measured: dp/dt max/min, SLVP, DLVP, HR and coronary flow. The oxidative stress biomarkers: TBARS, NO2, O2- and H2O2 were measured in coronary venous effluent. Isolated hearts were fixed and stained with H/E and Picro-sirius red staining. Psoriasis decreased cardiac contractility and relaxation and increased SLVP and DLVP at all perfusion pressure. Treatment with G.verum in psoriasis rats improved contractility and relaxation of the heart and rise SLVP and DLVP. In PSORI + GV group, the decrease of oxidative stress biomarkers were observed in comparison to PSORI group. Diameter and cross-section area of cardiomyocytes were increased in PSORI and PSORI + GV groups compared to the control. Collagen content was increased in PSORI group by 283% and in PSORI + GV group by 188% compared to control. Treatment with G.verum extract exhibited a positive effect on cardiac function, morphometry and redox state of heart of psoriatic rats.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3783-3798"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080475","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":"Altered cognitive function in obese patients: relationship to gut flora.","authors":"Mengyuan Deng, Fushan Tang, Zhaoqiong Zhu","doi":"10.1007/s11010-024-05201-y","DOIUrl":"10.1007/s11010-024-05201-y","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Obesity is a risk factor for non-communicable diseases such as cardiovascular disease and diabetes, which are leading causes of death and disability. Today, China has the largest number of overweight and obese people, imposing a heavy burden on China's healthcare system. Obesity adversely affects the central nervous system (CNS), especially cognitive functions such as executive power, working memory, learning, and so on. The gradual increase in adult obesity rates has been accompanied by a increase in childhood obesity rates. In the past two decades, the obesity rate among children under 5 years of age has increased from 32 to 42 million. If childhood obesity is not intervened in the early years, it will continue into adulthood and remain there for life. Among the potential causative factors, early lifestyle may influence the composition of the gut flora in childhood obesity, such as the rate and intake of high-energy foods, low levels of physical activity, may persist into adulthood, thus, early lifestyle interventions may improve the composition of the gut flora in obese children. Adipose Axis plays an important role in the development of obesity. Adipose tissue is characterized by increased expression of nucleoside diphosphate-linked molecule X-type motif 2 (NUDT2), amphiphilic protein AMPH genes, which encode proteins that all play important roles in the CNS. NUDT2 is associated with intellectual disability. Furthermore, amphiphysin (AMPH) is involved in glutamatergic signaling, ganglionic synapse development, and maturation, which is associated with mild cognitive impairment (MCI) and Alzheimer's disease (AD). All of the above studies show that obesity is closely related to cognitive decline in patients. Animal experiments have confirmed that obesity causes changes in cognitive function. For example, high-fat diets rich in long- and medium-chain saturated fatty acids may adversely affect cognitive function in obese mice. This process may be attributed to the Short-Chain Fatty Acid (SCFA)-rich high-fat diet (HFD) activating enterocyte TLR signaling, especially TLR-2 and TLR-4, altering the downstream MyD88-4 signaling, thereby impacting the downstream MyD88-NF-κB signaling cascade and up-regulating the levels of pro-inflammatory factors and lipopolysaccharide (LPS). These changes result in the loss of integrity of the intestinal mucosa and cause an imbalance in the internal environment. Obesity may lead to the disruption of the intestinal flora and damage the intestinal barrier function, causing intestinal flora dysbiosis. In recent years, a growing number of studies have investigated the relationship between obesity and the intestinal flora. For example, high-fat and high-sugar diets have been found to lead to the thinning of the mucus layer of the colon, a decrease in the number of tight junction proteins, and an increase in intestinal permeability in mice. Such changes alter the composition of intestinal microorganisms, allow endotox","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3553-3567"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12095350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399209","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":"Effects of FAP+ fibroblasts on cell proliferation migration and immunoregulation of esophageal squamous carcinoma cells through the CXCL12/CXCR4 axis.","authors":"Lijuan Duan, Shasha Cao, Fang Zhao, Xianjuan Du, Zhaowei Gao, Xiaoxiao Wang, Fang Bian","doi":"10.1007/s11010-025-05226-x","DOIUrl":"10.1007/s11010-025-05226-x","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) secrete and synthesize fibroblast activation protein (FAP), which could promote proliferation and immunosuppression of multiple cancers including esophageal squamous cell carcinoma (ESCC). CXCL12/CXCR4 signaling could be revitalized by CAFs in cancer cells. Nevertheless, the significance of this interaction in ESCC has yet to be elucidated. Herein, we investigated whether FAP⁺ CAF cells could promote ESCC cells proliferation, migration and regulate immunity through the CXCL12/CXCR4 pathway in vitro and in vivo. The protein expression level of FSP1, FAP, CD8+ and Ki-67 in different sample was estimated by IHC and western blot. qPCR was used to quantify the mRNA level of FSP1, FAP, CD8+ and Ki-67 in different sample. The cell viability, proliferation, migration and invasion of different sample were evaluated by CCK-8, EdU staining, wound healing assay and Transwell assay, respectively. The ELISA was carried out to measure the protein level of IFN-γ, TNF-α, GZMB and IL-2. ESCC xenograft mice model was established to assess the impact of FAP+ CAF. FSP1, FAP, CD8+ and Ki-67 are greatly up-regulated in hESCC tissues. Through CXCL12/CXCR4 axis, FAP-positive CAF was capable of promoting the cell proliferation, migration and invasion of ESCC tumor cells and preventing the CD8+ T cells from secreting cytokine. Blocking this signaling with selective CXCR4 antagonist could counteract the effects caused by high-expression of FAP. FAP+ CAFs could inhibit the occurrence and development of tumors. These results indicated that FAP-positive CAF have an impact on cell proliferation migration and immunoregulation of ESCC through the CXCL12/CXCR4 axis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"3841-3855"},"PeriodicalIF":3.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399211","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}