American journal of physiology. Cell physiology最新文献

{"title":"Animal models of haploinsufficiency revealed the isoform-specific role of GSK-3 in HFD-induced obesity and glucose intolerance.","authors":"Manisha Gupte, Prachi Umbarkar, Jacob Lemon, Sultan Tousif, Hind Lal","doi":"10.1152/ajpcell.00552.2024","DOIUrl":"10.1152/ajpcell.00552.2024","url":null,"abstract":"<p><p>Glycogen synthase kinase 3 (GSK-3), a serine-threonine kinase with two isoforms (α and β) is implicated in the pathogenesis of type 2 diabetes mellitus (T2D). Recently, we reported the isoform-specific role of GSK-3 in T2D using homozygous GSK-3α/β knockout mice. Although the homozygous inhibition models are idealistic in a preclinical setting, they do not mimic the inhibition seen with pharmacological agents. Hence, in this study, we sought to investigate the dose-response effect of GSK-3α/β inhibition in the pathogenesis of obesity-induced T2D. Specifically, to gain insight into the dose-response effect of GSK-3 isoforms in T2D, we generated tamoxifen-inducible global GSK-3α/β heterozygous mice. GSK-3α/β heterozygous and control mice were fed a high-fat diet (HFD) for 16 wk. At baseline, the body weight and glucose tolerance of GSK-3α heterozygous and controls were comparable. In contrast, at baseline, a modest but significantly higher body weight (higher lean mass) was seen in GSK-3β heterozygous compared with controls. Post-HFD, GSK-3α heterozygous and controls displayed a comparable phenotype. However, GSK-3β heterozygous were significantly protected against obesity-induced glucose intolerance. Interestingly, the improved glucose tolerance in GSK-3β heterozygous animals was dampened with chronic HFD-feeding, likely due to significantly higher fat mass and lower lean mass in the GSK-3β animals. These findings suggest that GSK-3β is the dominant isoform in glucose metabolism. However, to avail the metabolic benefits of GSK-3β inhibition, it is critical to maintain a healthy weight.<b>NEW & NOTEWORTHY</b> The precise isoform-specific role of GSK-3 in obesity-induced glucose intolerance is unclear. To overcome the limitations of pharmacological GSK-3 inhibitors (not isoform-specific) and tissue-specific genetic models, in the present study, we created novel inducible heterozygous mouse models of GSK-3 inhibition that allowed us to delete the gene globally in an isoform-specific and temporal manner to determine the isoform-specific role of GSK-3 in obesity-induced glucose intolerance.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1349-C1358"},"PeriodicalIF":5.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339320","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":"Homeostatic regulation of brain activity: from endogenous mechanisms to homeostatic nanomachines.","authors":"Caterina Michetti, Fabio Benfenati","doi":"10.1152/ajpcell.00470.2024","DOIUrl":"10.1152/ajpcell.00470.2024","url":null,"abstract":"<p><p>After the initial concepts of the constancy of the internal milieu or homeostasis, put forward by Claude Bernard and Walter Cannon, homeostasis emerged as a mechanism to control oscillations of biologically meaningful variables within narrow physiological ranges. This is a primary need in the central nervous system that is continuously subjected to a multitude of stimuli from the internal and external environments that affect its function and structure, allowing to adapt the individual to the ever-changing daily conditions. Preserving physiological levels of activity despite disturbances that could either depress neural computation or excessively stimulate neural activity is fundamental, and failure of these homeostatic mechanisms can lead to brain diseases. In this review, we cover the role and main mechanisms of homeostatic plasticity involving the regulation of excitability and synaptic strength from the single neuron to the network level. We analyze the relationships between homeostatic and Hebbian plasticity and the conditions under which the preservation of the excitatory/inhibitory balance fails, triggering epileptogenesis and eventually epilepsy. Several therapeutic strategies to cure epilepsy have been designed to strengthen homeostasis when endogenous homeostatic plasticity mechanisms have become insufficient or ineffective to contrast hyperactivity. We describe \"on demand\" gene therapy strategies, including optogenetics, chemogenetics, and chemo-optogenetics, and particularly focus on new closed loop sensor-actuator strategies mimicking homeostatic plasticity that can be endogenously expressed to strengthen the homeostatic defenses against brain diseases.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1384-C1399"},"PeriodicalIF":5.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455974","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":"Innate players in Th2 and non-Th2 asthma: emerging roles for the epithelial cell, mast cell, and monocyte/macrophage network.","authors":"Johanna Kotrba, Ilka Müller, Alexander Pausder, Aaron Hoffmann, Belinda Camp, Julia D Boehme, Andreas J Müller, Jens Schreiber, Dunja Bruder, Sascha Kahlfuss, Anne Dudeck, Sabine Stegemann-Koniszewski","doi":"10.1152/ajpcell.00488.2024","DOIUrl":"10.1152/ajpcell.00488.2024","url":null,"abstract":"<p><p>Asthma is one of the most common chronic respiratory diseases and is characterized by airway inflammation, increased mucus production, and structural changes in the airways. Recently, there is increasing evidence that the disease is much more heterogeneous than expected, with several distinct asthma endotypes. Based on the specificity of T cells as the best-known driving force in airway inflammation, bronchial asthma is categorized into T helper cell 2 (Th2) and non-Th2 asthma. The most studied effector cells in Th2 asthma include T cells and eosinophils. In contrast to Th2 asthma, much less is known about the pathophysiology of non-Th2 asthma, which is often associated with treatment resistance. Besides T cells, the interaction of myeloid cells such as monocytes/macrophages and mast cells with the airway epithelium significantly contributes to the pathogenesis of asthma. However, the underlying molecular regulation and particularly the specific relevance of this cellular network in certain asthma endotypes remain to be understood. In this review, we summarize recent findings on the regulation of and complex interplay between epithelial cells and the \"nonclassical\" innate effector cells mast cells and monocytes/macrophages in Th2 and non-Th2 asthma with the ultimate goal of providing the rationale for future research into targeted therapy regimens.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1373-C1383"},"PeriodicalIF":5.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455975","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":"Unlocking the mechanisms of muscle fatigue: insights from the Marion J. Siegman Award Lectures.","authors":"Arthur J Cheng, Nathaniel J Andrews, Thomas J Hawke","doi":"10.1152/ajpcell.00620.2024","DOIUrl":"10.1152/ajpcell.00620.2024","url":null,"abstract":"","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1347-C1348"},"PeriodicalIF":5.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-induced TIMAP upregulation in endothelial cells and TIMAP-dependent tumor angiogenesis.","authors":"Salah Aburahess, Laiji Li, Aashiq Hussain, Marya Obeidat, Parnian Alavi, Abul K Azad, Nadia Jahroudi, Barbara J Ballermann","doi":"10.1152/ajpcell.00054.2024","DOIUrl":"10.1152/ajpcell.00054.2024","url":null,"abstract":"<p><p>TGFβ-inhibited membrane associated protein (TIMAP), the endothelial cell-predominant protein phosphatase 1β regulatory subunit also known as PPP1R16B, promotes in vitro endothelial cell proliferation and angiogenic sprouting. TIMAP was first identified as a target of TGF-β1-mediated repression, but the molecular pathways regulating its expression in endothelial cells are not well-defined. This study examined the role of bone morphogenetic factor 9 (BMP9), hypoxia, and angiogenic growth factors in the regulation of TIMAP expression and determined whether TIMAP plays a role in tumor angiogenesis and growth in vivo. BMP9, which potently activated the SMAD1/5/8 pathway in endothelial cells, significantly reduced TIMAP mRNA and protein expression. Conversely, hypoxia and the prolyl hydroxylase inhibitor Roxadustat raised TIMAP mRNA and protein levels by inhibiting the SMAD1/5/8 pathway. Angiogenic growth factors, including VEGFA and IGF-I, raised endothelial TIMAP levels partly by attenuating SMAD1/5/8 pathway activation, but also through SMAD1/5/8-independent mechanisms. Cultured breast cancer E0771 cells released mediators that raised TIMAP expression in endothelial cells, effects that were inhibited by the VEGF inhibitor Sunitinib in conjunction with the IGF-1 inhibitor Picropodophyllin. In the mouse E0771 breast cancer model in vivo, tumor growth and tumor angiogenesis were markedly attenuated in TIMAP deficient, compared with wild-type littermates. These findings indicate that TIMAP plays a critical proangiogenic function during tumor angiogenesis in vivo, likely through hypoxia-driven inhibition of the SMAD1/5/8 pathway and through the elaboration of angiogenic growth factors by tumor cells.<b>NEW & NOTEWORTHY</b> The protein phosphatase 1 regulatory subunit TGFβ-inhibited membrane associated protein (TIMAP), known to activate AKT in endothelial cells (EC), was shown here to be repressed by bone morphogenetic factor 9 (BMP9). Hypoxia and angiogenic growth factors induced TIMAP expression by inhibiting the BMP9 pathway. In a mouse breast cancer model, TIMAP deletion inhibited tumor angiogenesis and tumor growth. Therefore, the proangiogenic functions of TIMAP are induced by hypoxia and angiogenic growth factors.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1359-C1372"},"PeriodicalIF":5.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human skeletal muscle possesses an epigenetic memory of high intensity interval training.","authors":"Andrea M Pilotto, Daniel C Turner, Raffaele Mazzolari, Emanuela Crea, Lorenza Brocca, Maria Antonietta Pellegrino, Danilo Miotti, Roberto Bottinelli, Adam P Sharples, Simone Porcelli","doi":"10.1152/ajpcell.00423.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00423.2024","url":null,"abstract":"<p><strong>Introduction: </strong>Human skeletal muscle displays an epigenetic memory of resistance exercise induced by hypertrophy. It is unknown, however, whether high-intensity interval training (HIIT) also evokes an epigenetic muscle memory. This study employed repeated training intervention interspersed with a detraining period to assess epigenetic memory of HIIT.</p><p><strong>Methods: </strong>Twenty healthy subjects (25±5yrs) completed two HIIT interventions (training and retraining) lasting 2 months, separated by 3 months of detraining. Measurements at baseline, after training, detraining and retraining included maximal oxygen consumption (V̇ O_2max). Vastus lateralis biopsies were taken for genome-wide DNA methylation and targeted gene expression analyses.</p><p><strong>Results: </strong>V̇ O_2max improved during training and retraining (p<0.001) without differences between interventions (p>0.58). Thousands of differentially methylated positions (DMPs) predominantly demonstrated a hypomethylated state after training, retained even after 3-months exercise cessation and into retraining. Five genes; ADAM19, INPP5a, MTHFD1L, CAPN2, SLC16A3 possessed differentially methylated regions (DMRs) with retained hypomethylated memory profiles and increased gene expression. The retained hypomethylation during detraining was associated with an enhancement in expression of the same genes even after 3 months of detraining. SLC16A3, INPP5a, CAPN2 are involved in lactate transport and calcium signaling.</p><p><strong>Conclusions: </strong>Despite similar physiological adaptations between training and retraining, memory profiles were found at epigenetic and gene expression level, characterized by retained hypomethylation and increased gene expression after training into long-term detraining and retraining. These genes were associated with calcium signaling and lactate transport. Whilst significant memory was not observed in physiological parameters, our novel findings indicate that human skeletal muscle possesses an epigenetic memory of HIIT.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680592","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":"Cultured Primary Turtle Hepatocytes: A Cellular Model for The Study of Temperature and Anoxia.","authors":"Alexander M Myrka, Ryan Frost, Domenic Distefano, Sergey V Plotnikov, Leslie T Buck","doi":"10.1152/ajpcell.00510.2023","DOIUrl":"https://doi.org/10.1152/ajpcell.00510.2023","url":null,"abstract":"<p><p>Turtle hepatocytes are a non-excitable model for metabolic depression during low-temperature and/or anoxic overwintering conditions. Cytoskeletal structure and mitochondrial distribution are continuously modified in cells, and we hypothesized that metabolic depression would inhibit such processes as cell attachment and spreading and promote withdrawal of cell protrusions and peripheral mitochondria. After developing a methodology for culturing painted turtle hepatocytes, maintenance of cell attachment after a media change, and 2D area, were used as indicators of structural rearrangement and spreading/volume. These were measured after incubating cells at varying temperatures and with or without the inclusion of cyanide (chemical proxy for anoxia). Experiments were performed using cells from 22°C- or 5°C-acclimated turtles. Live-cell imaging was used to monitor the effect of cyanide exposure on distribution of mitochondria. We also acclimated cultured cells from 22°C-acclimated turtles to 4°C <i>in vitro</i> and scored withdrawal of protrusions. Only cells isolated from 5°C-acclimated turtles and incubated at 4°C had reduced attachment to fibronectin substrate, but cyanide exposure had no effect. These cells also had a 24% smaller 2D area than those from 22°C-acclimated turtles. There was no change in mitochondrial distribution during cyanide perfusion. Finally, 4°C acclimation <i>in vitro</i> resulted in withdrawal of protrusions over 14 days. Taken together with the results from cells acclimated to low temperature <i>in vivo</i>, this suggests inhibition of structural rearrangement and protrusion stability by low temperature acclimation, but not cyanide exposure. Our cultured primary hepatocyte system will facilitate further study of the role of structural dynamics in reversible metabolic depression.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142650561","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":"Cohesin <i>rad21</i> mutation dysregulates erythropoiesis and granulopoiesis output within the whole kidney marrow of adult zebrafish.","authors":"Gregory Gimenez, Maggie L Kalev-Zylinska, Ian Morison, Stefan K Bohlander, Julia A Horsfield, Jisha Antony","doi":"10.1152/ajpcell.00657.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00657.2024","url":null,"abstract":"<p><p>Cohesin complex is essential for cell division and for regulating cell type-specific gene expression programs. Mutations in genes encoding the cohesin subunits are associated with hematological malignancies, pre-leukemia and clonal hematopoiesis of indeterminate potential. In this study, we examined how cohesin mutation impacts hematopoiesis using adult zebrafish that carry heterozygous germline nonsense mutation in the cohesin subunit, <i>rad21</i> (<i>rad21+/-</i>) that is orthologous to human <i>RAD21</i>. Single cell RNA sequencing analyses showed that adult zebrafish harboring <i>rad21+/-</i> mutation exhibit significant transcriptional dysregulation within the whole kidney marrow and have altered erythroid and granulocyte output. Erythroid progenitors were expanded in <i>rad21+/-</i> and erythroid differentiation was altered. The expression profile of several erythroid genes, including <i>gata1a,</i> was dysregulated in <i>rad21+/-</i> erythroid cells. Mature granulocyte population declined in <i>rad21+/-</i>, and the transcriptional program of granulocytes was impaired but granulocytic maturation was maintained. Granulocytes from <i>rad21+/-</i> showed upregulation of stress hematopoiesis factor, <i>cebpb</i>. These findings show that normal <i>rad21</i> is required to maintain steady erythropoiesis and granulopoiesis in the adult zebrafish marrow.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643240","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":"No detectable loss of myonuclei from human muscle fibers after six weeks of immobilization following an Achilles tendon rupture.","authors":"Oscar Horwath, Kristoffer Toldnes Cumming, Einar Eftestøl, Björn Ekblom, Paul Ackermann, Truls Raastad, Kristian Gundersen, Niklas Psilander","doi":"10.1152/ajpcell.00692.2024","DOIUrl":"https://doi.org/10.1152/ajpcell.00692.2024","url":null,"abstract":"<p><p>Muscle disuse has rapid and debilitating effects on muscle mass and overall health, making it an important issue from both scientific and clinical perspectives. However, the myocellular adaptations to muscle disuse are not yet fully understood, particularly those related to the myonuclear permanence hypothesis. Therefore, in this study, we assessed fiber size, number of myonuclei, satellite cells, and capillaries in human <i>gastrocnemius</i> muscle after a period of immobilization following an Achilles tendon rupture. Six physically active patients (5M/1F, 43 {plus minus} 15 years) were recruited to participate after sustaining an acute unilateral Achilles tendon rupture. Muscle biopsies were obtained from the lateral part of the <i>gastrocnemius</i> before and after six weeks of immobilization using a plaster cast and orthosis. Muscle fiber characteristics were analyzed in tissue cross-sections and isolated single fibers using immunofluorescence and high-resolution microscopy. Immobilization did not change muscle fiber type composition nor cross-sectional area of type I or type II fibers, but muscle fiber volume tended to decline by 13% (p=0.077). After immobilization, the volume per myonucleus was significantly reduced by 20% (p=0.008). Myonuclei were not lost in response to immobilization but tended to increase in single fibers and type II fibers. No significant changes were observed for satellite cells or capillaries. Myonuclei were not lost in the <i>gastrocnemius</i> muscle after a prolonged period of immobilization, which may provide support to the myonuclear permanence hypothesis in human muscle. Capillaries remained stable throughout the immobilization period, whereas the response was variable for satellite cells, particularly in type II fibers.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142638537","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":"Role of myofiber-specific FoxP1 in pancreatic cancer-induced muscle wasting.","authors":"Martin M Schonk, Jeremy B Ducharme, Daria Neyroud, Rachel L Nosacka, Haley O Tucker, Sarah M Judge, Andrew R Judge","doi":"10.1152/ajpcell.00701.2024","DOIUrl":"10.1152/ajpcell.00701.2024","url":null,"abstract":"<p><p>Cancer cachexia affects up to 80% of cancer patients and results in reduced quality of life and survival. We previously demonstrated that the transcriptional repressor Forkhead box P1 (FoxP1) is upregulated in skeletal muscle of cachectic mice and people with cancer, and when overexpressed in skeletal muscle is sufficient to induce pathological features characteristic of cachexia. However, the role of myofiber-derived FoxP1 in both normal muscle physiology and cancer-induced muscle wasting remains largely unexplored. To address this gap, we generated a conditional mouse line with myofiber-specific ablation of FoxP1 (FoxP1^SkmKO) and found that in cancer-free mice, deletion of FoxP1 in skeletal myofibers resulted in increased myofiber size in both males and females, with a significant increase in muscle mass in males. In response to murine KPC pancreatic tumor burden, we found that myofiber-derived FoxP1 is required for cancer-induced muscle wasting and diaphragm muscle weakness in male mice. In summary, our findings identify myofiber-specific FoxP1 as a negative regulator of skeletal muscle with sex-specific differences in the context of cancer.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612360","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}