American journal of physiology. Cell physiology最新文献

{"title":"Diurnal differences in postprandial glucose and triglyceride metabolism reveal metabolic flexibility and resilience.","authors":"Rebecca Dörner, Franziska A Hägele, Shauna D O'Donovan, Jennifer L Miles-Chan, Manfred J Müller, Anja Bosy-Westphal","doi":"10.1152/ajpcell.00102.2025","DOIUrl":"10.1152/ajpcell.00102.2025","url":null,"abstract":"<p><p>The study investigated the diurnal variance in metabolic resilience (i.e., the robustness, the recovery, and reorientation of metabolism) and metabolic flexibility in glucose and fat oxidation rates to three identical test meals. Eight young, healthy subjects consumed identical liquid mixed meals three times a day (33% of energy requirement each), followed by a defined bout of physical activity conducted in a whole room indirect calorimeter to continuously assess energy expenditure and postprandial changes in substrate oxidation rates as a measure of metabolic flexibility. A mathematical metabolic resilience model was used to analyze the postprandial blood parameters. Throughout the day, postprandial glucose area under the curve (AUC) increased (means ± SD, breakfast 17.3 ± 2.4 vs. dinner 20.8 ± 2.0 g/180 min; <i>P</i> < 0.001), whereas triglyceride AUC decreased (breakfast 434 ± 158 vs. dinner 365 ± 104 mg/180 min; <i>P</i> = 0.039) at identical insulin AUC and energy balance. Fat oxidation increased from breakfast 24.8 ± 8.7 to dinner 28.0 ± 8.7 g/180 min (<i>P</i> = 0.029), whereas the respiratory exchange ratio declined from 0.035 ± 0.026 to 0.012 ± 0.029 (<i>P</i> = 0.005). The metabolic resilience model reveals a diurnal increase in the rate of lipolysis of circulating triglycerides at a concomitant decrease in the rate of exogenous and endogenous triglyceride appearance. Meal-to-meal changes in glucose AUC indicate rising insulin resistance during the day. However, this reflects a resilient metabolism that shifts to triglyceride metabolism in the evening while maintaining insulin AUC and energy balance.<b>NEW & NOTEWORTHY</b> Conventionally, postprandial tests have focused exclusively on glucose metabolism. The integration of a mixed meal computational model with substrate oxidation rates facilitates the assessment of the interplay between glucose and lipid metabolism, thereby determining metabolic resilience under physiological conditions. Throughout the day, metabolic resilience is characterized by increased triglyceride lipolysis with a decreased rate of triglyceride appearance from the gut and an increased basal rate of endogenous triglycerides from the liver, whereas metabolic flexibility decreases.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1383-C1388"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143646945","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":"Fibronectin-dependent integrin signaling drives EphA2 expression in vascular smooth muscle cells.","authors":"Brenna Pearson-Gallion, Alexandra C Finney, Matthew L Scott, Zachary Connelly, Shafiul Alam, Jonette M Peretik, Cyrine Ben Dhaou, Md Shenuarin Bhuiyan, James G Traylor, William F DeGrado, Hyunil Jo, Xiuping Yu, Oren Rom, Christopher B Pattillo, Nirav Dhanesha, Arif Yurdagul, A Wayne Orr","doi":"10.1152/ajpcell.01021.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.01021.2024","url":null,"abstract":"<p><p>Vascular smooth muscle cells undergo a phenotypic shift to a \"synthetic\" phenotype during atherosclerosis characterized by downregulation of contractile markers and augmented proliferation, migration, and extracellular matrix deposition. While absent in contractile smooth muscle cells, the receptor tyrosine kinase EphA2 shows enhanced expression in synthetic vascular smooth muscle in vitro and in atherosclerotic plaques in vivo. EphA2 deletion in atheroprone <i>ApoE</i> knockout mice reduces plaque size, fibrous tissue, and smooth muscle content. However, the mechanisms regulating smooth muscle EphA2 expression remain unknown. Although serum strongly induces EphA2 expression, individual growth factors and insulin all failed to stimulate EphA2 expression in smooth muscle cells. In contrast, adhesion to fibronectin stimulated the expression of EphA2, while blunting serum-induced fibronectin deposition attenuated EphA2 expression, suggesting a critical role for fibronectin signaling. Fibronectin binds to a subset of extracellular matrix-binding integrins, and blocking fibronectin-integrin interactions or inhibiting specific fibronectin-binding integrins both attenuated EphA2 expression. Furthermore, pharmacological inhibition of fibronectin-binding integrins significantly reduced EphA2 expression in atherosclerotic plaques. RNA sequencing analysis of fibronectin-associated gene expression pointed to NF-κB as a likely transcription factor mediating fibronectin-responsive genes. Adhesion to fibronectin enhanced NF-κB activation in smooth muscle cells and inhibiting NF-κB blunted EphA2 expression associated with fibronectin. In addition, chromatin immunoprecipitation showed that NF-κB directly interacts with the EphA2 promoter, and mutating this site blunts fibronectin-dependent EphA2 promoter activity. Together these data identify a novel role for fibronectin-dependent integrin signaling in the induction of smooth muscle EphA2 expression.<b>NEW & NOTEWORTHY</b> Here, we demonstrate a novel interplay between cell-cell and cell-matrix adhesions, showing that fibronectin-dependent integrin signaling promotes NF-κB activation and interaction with the EphA2 promoter to drive smooth muscle EphA2 expression, whereas integrin inhibition attenuates EphA2 expression in atherosclerotic plaques in vivo. Although this relationship has clear implications on smooth muscle fibroproliferative remodeling in atherosclerosis, the matrix-specific regulation of EphA2 expression may impact a variety of pathological conditions.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 5","pages":"C1623-C1636"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964725","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":"Trpv4-mediated mechanotransduction regulates the differentiation of valvular interstitial cells to myofibroblasts: implications for aortic valve stenosis.","authors":"Pritha Mukherjee, Manisha Mahanty, Bidisha Dutta, Suneha G Rahaman, Karunakaran R Sankaran, Zhenguo Liu, Shaik O Rahaman","doi":"10.1152/ajpcell.00977.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00977.2024","url":null,"abstract":"<p><p>As aortic valve stenosis (AVS) progresses, the valve tissue also stiffens. This increase in tissue stiffness causes the valvular interstitial cells (VICs) to transform into myofibroblasts in response. VIC-to-myofibroblast differentiation is critically involved in the development of AVS. Herein, we investigated the role of mechanosensitive Ca²⁺-permeant transient receptor potential vanilloid 4 (Trpv4) channels in matrix stiffness- and transforming growth factor β1 (TGFβ1)-induced VIC-myofibroblast activation. We confirmed Trpv4 functionality in primary mouse wild-type VICs compared with Trpv4 null VICs using live Ca²⁺ influx detection during application of its selective agonist and antagonist. Using physiologically relevant hydrogels of varying stiffness that respectively mimic healthy or diseased aortic valve tissue stiffness, we found that genetic ablation of Trpv4 blocked matrix stiffness- and TGFβ1-induced VIC-myofibroblast activation as determined by changes in morphology, alterations of expression of α-smooth muscle actin, and modulations of F-actin generation. Our results showed that N-terminal residues 30-130 in Trpv4 were crucial for cellular force generation and VIC-myofibroblast activation, while deletion of residues 1-30 had no noticeable negative effect on these processes. Collectively, these data suggest a differential regulatory role for Trpv4 in stiffness/TGFβ1-induced VIC-myofibroblast activation. Our data further showed that Trpv4 regulates stiffness/TGFβ1-induced PI3K-AKT activity that is required for VIC-myofibroblast differentiation and cellular force generation, suggesting a mechanism by which Trpv4 activity regulates VIC-myofibroblast activation. Altogether, these data identify a novel role for Trpv4 mechanotransduction in regulating VIC-myofibroblast activation, implicating Trpv4 as a potential therapeutic target to slow and/or reverse AVS development.<b>NEW & NOTEWORTHY</b> Aortic valve stenosis (AVS) progression involves stiffened valve tissue, driving valvular interstitial cells (VICs) to transform into myofibroblasts. This study highlights the role of Trpv4 channels in VIC activation triggered by matrix stiffness and TGFß1. Using hydrogels mimicking healthy and diseased valves, researchers found that Trpv4 regulates cellular force generation and differentiation via PI3K-AKT activity. These findings identify Trpv4 as a potential therapeutic target to slow or reverse AVS progression.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 5","pages":"C1558-C1570"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143957250","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":"Oxygen dynamics and delivery strategies to enhance beta cell replacement therapy.","authors":"Kuang-Ming Shang, Tomoharu Suzuki, Hiroyuki Kato, Taro Toyoda, Yu-Chong Tai, Hirotake Komatsu","doi":"10.1152/ajpcell.00984.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00984.2024","url":null,"abstract":"<p><p>Beta cell replacement therapy via pancreatic islet transplantation offers a promising treatment for type 1 diabetes as an alternative to insulin injections. However, posttransplantation oxygenation remains a critical challenge; isolated islets from donors lose vascularity and rely on slow oxygen diffusion for survival until revascularization occurs in the host tissue. This often results in significant hypoxia-induced acute graft loss. Overcoming the oxygenation barrier is crucial for advancing islet transplantation. This review is structured in three sections: the first examines oxygen dynamics in islet transplantation, focusing on factors affecting oxygen supply, including vascularity. It highlights oxygen dynamics specific to both transplant sites and islet grafts, with particular attention to extrahepatic sites such as subcutaneous tissue. The second section explores current oxygen delivery strategies, categorized into two main approaches: augmenting oxygen supply and enhancing effective oxygen solubility. The final section addresses key challenges, such as the lack of a clearly defined oxygen threshold for islet survival and the limited precision in measuring oxygen levels within small islet constructs. Recent advancements addressing these challenges are introduced. By deepening the understanding of oxygen dynamics and identifying current obstacles, this review aims to guide the development of innovative strategies for future research and clinical applications. These advancements are anticipated to enhance transplantation outcomes and bring us closer to a cure for type 1 diabetes.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"328 5","pages":"C1667-C1684"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955780","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":"Intestinal luminal anion transporters and their interplay with gut microbiome and inflammation.","authors":"Nazim Husain, Anoop Kumar, Arivarasu N Anbazhagan, Ravinder K Gill, Pradeep K Dudeja","doi":"10.1152/ajpcell.00026.2025","DOIUrl":"10.1152/ajpcell.00026.2025","url":null,"abstract":"<p><p>The intestine, as a critical interface between the external environment and the internal body, plays a central role in nutrient absorption, immune regulation, and maintaining homeostasis. The intestinal epithelium, composed of specialized epithelial cells, harbors apical anion transporters that primarily mediate the transport of chloride and bicarbonate ions, essential for maintaining electrolyte balance, pH homeostasis, and fluid absorption/secretion. In addition, the intestine hosts a diverse population of gut microbiota that plays a pivotal role in various physiological processes including nutrient metabolism, immune regulation, and maintenance of intestinal barrier integrity, all of which are critical for host gut homeostasis and health. The anion transporters and gut microbiome are intricately interconnected, where alterations in one can trigger changes in the other, leading to compromised barrier integrity and increasing susceptibility to pathophysiological states including gut inflammation. This review focuses on the interplay of key apical anion transporters including Down-Regulated in Adenoma (DRA, SLC26A3), Putative Anion Transporter-1 (PAT1, SLC26A6), and Cystic Fibrosis Transmembrane Conductance Regulator [CFTR, ATP-binding cassette subfamily C member 7 (ABCC7)] with the gut microbiome, barrier integrity, and their relationship to gut inflammation.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1455-C1472"},"PeriodicalIF":5.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565777","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":"Orai channel pharmacological manipulation reduces metabolic flexibility in cardiac fibroblasts.","authors":"Patricia Da Silva Pantoja Newman, Amandeep Bajwa, Agnese De Mario, Cristina Mammucari, Salvatore Mancarella","doi":"10.1152/ajpcell.00822.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00822.2024","url":null,"abstract":"<p><p>Cardiac fibroblasts (CF) play a crucial role in regulating normal heart function and are also involved in the pathological remodeling of the heart that occurs due to hypertension, myocardial infarction, and heart failure. Metabolic changes in fibroblasts are key drivers in the progression of these diseases. Calcium (Ca²⁺) signaling and Ca²⁺ ion channels control many functions of fibroblasts. Orai Ca²⁺ channels are abundantly expressed in fibroblasts; however, their exact role is not yet fully understood. This study examined the role of Orai Ca²⁺ channels in maintaining Ca²⁺ homeostasis within organelles and in energy production in CF. Chronic inhibition of Orai activity altered the expression levels of major metabolic enzymes, affecting the overall metabolic state of the cells. Orai channels are required to refill the endoplasmic reticulum (ER) store. Acute Orai channel activity inhibition reduced Ca²⁺ content in both the ER and mitochondria and was associated with the impaired ability to use glucose as a primary energy source. These results have significant implications for understanding the role of Orai-dependent Ca²⁺ entry in maintaining organellar Ca²⁺ homeostasis and cellular metabolic flexibility, sparking further research in this area.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960804","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":"Are you listening - Cellular Signaling in ECM-Driven Disease.","authors":"Alexander Nyström","doi":"10.1152/ajpcell.00337.2025","DOIUrl":"https://doi.org/10.1152/ajpcell.00337.2025","url":null,"abstract":"","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953456","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":"Epigenetic Modulation of Cisplatin Sensitivity by the M6A-Linked ceRNA Network in Non-Small Cell Lung Cancer.","authors":"Qi Wang, He Yan, Jing Zhang, Jie Zhang, Xiaomin Su, Zhenzhong Su","doi":"10.1152/ajpcell.00881.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00881.2024","url":null,"abstract":"<p><p>Cisplatin resistance significantly impedes effective treatment of non-small cell lung cancer (NSCLC). This study investigates the role of the M6A-related circFUT8/miR-185-5p/HNRNPC competing endogenous RNA (ceRNA) axis in NSCLC cisplatin resistance. Bioinformatics analysis identified HNRNPC, a critical M6A modification-related gene, as a promoter of NSCLC proliferation and metastasis. Our <i>in vitro</i> and <i>in vivo</i> experiments reveal that circFUT8 upregulates HNRNPC by sponging miR-185-5p, thus enhancing NSCLC cell proliferation, migration, and invasion while reducing apoptosis and sensitivity to cisplatin. These findings highlight the circFUT8/miR-185-5p/HNRNPC axis as a potential target to overcome chemoresistance in NSCLC.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144061937","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":"Mechano-metabolism: Recent Findings on the Intersection of Cell Adhesion, Cell Migration, and Metabolism.","authors":"Emily D Fabiano, Jenna M Poole, Cynthia A Reinhart-King","doi":"10.1152/ajpcell.00892.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00892.2024","url":null,"abstract":"<p><p>Chemical and mechanical cues within the extracellular matrix (ECM) can initiate intracellular signaling that changes an array of fundamental cell functions. In recent work, studies of cell-ECM adhesion have deepened to include the influence of the physical ECM on cell metabolism. Since many biological processes involve metabolic programs, changes to cellular metabolism in response to cues in the ECM can have marked effects on cell health. In this review, we describe molecular mechanisms associated with cell-ECM adhesion that are key players in metabolism-induced changes to cell behaviors, including migration. We first review how changes to metabolite availability in the extracellular environment or manipulation of metabolic machinery in cells impact focal adhesions. We then connect this work to recent findings regarding the reverse relationship, namely how the manipulation of focal adhesion proteins or integrins feeds back to alter cell metabolism. Finally, we consider the latest findings from studies that describe how the mechanical properties of the ECM, primarily stiffness and confinement, alter cellular metabolism. We identify key areas of future investigation that may elucidate the molecular drivers that permit cells to respond to mechanical and chemical ECM cues by reprogramming their metabolism to better inform future diagnostics and therapeutics for disease states.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952249","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":"Mechanistic Insights into Hippo-YAP Pathway Activation for Enhanced DFU Healing.","authors":"Shaochun Zhang, Ye Wang, Xuesong Xiong, Jili Xing, Ke Jing","doi":"10.1152/ajpcell.01067.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.01067.2024","url":null,"abstract":"<p><p>With the increasing prevalence of diabetes, diabetic foot ulcers (DFU) have become a global health challenge, significantly impacting patients' quality of life and placing a substantial burden on healthcare systems. Among various immune cell subsets, M2-polarized macrophages play a pivotal role in tissue repair and inflammation resolution. This study employs single-cell RNA sequencing (scRNA-seq) and bulk RNA sequencing to comprehensively investigate the role of the TFAP2A-LIFR-Hippo-YAP signaling axis in regulating macrophage M2 polarization and its critical function in DFU wound healing. Through scRNA-seq analysis, we identified nine major immune cell subsets in DFU samples, with macrophages emerging as key regulatory cells. In vitro experiments further confirmed that TFAP2A promotes macrophage M2 polarization (evidenced by increased expression of the M2 marker ARG1) and ameliorates endothelial dysfunction by enhancing tube formation, improving migration capacity, and upregulating relevant proteins such as VCAM-1. Moreover, TFAP2A serves as a central regulatory gene for macrophage function in DFU by upregulating LIFR expression and activating the Hippo-YAP signaling pathway, thereby inducing M2 polarization and mitigating endothelial dysfunction. Mouse model experiments further demonstrated that the TFAP2A-LIFR-Hippo-YAP signaling axis accelerates DFU wound healing through the induction of macrophage M2 polarization. This study unveils a novel immunoregulatory role of TFAP2A in DFU and provides a promising therapeutic target for the treatment of chronic diabetic wounds.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143956397","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}