American journal of physiology. Cell physiology最新文献

{"title":"Correction for Xiong et al., volume 329, 2025, p. C1624-C1641.","authors":"","doi":"10.1152/ajpcell.00924.2024_COR","DOIUrl":"https://doi.org/10.1152/ajpcell.00924.2024_COR","url":null,"abstract":"","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"330 6","pages":"C1668"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136698","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":"Individual and combined effects of wheel running and ischemic preconditioning in protecting the rat heart from reperfusion injury.","authors":"Jyotsna Mishra, Cathryn Krier, Matthew Cavanaugh, Anika Asija, John E Baker, Wai-Meng Kwok, Amadou K S Camara, Robert H Fitts","doi":"10.1152/ajpcell.00108.2026","DOIUrl":"10.1152/ajpcell.00108.2026","url":null,"abstract":"<p><p>It is well known that exercise training (TRN) and ischemic preconditioning (IPC) reduce cardiomyocyte (CM) death following ischemia and reperfusion (IR), but it is unknown if protection can be elicited by moderate exercise TRN or if the effects of TRN and IPC summate to generate greater protection than either protocol alone. To address these questions, we used wheel running, a moderate-intensity paradigm, to TRN male and female rats, and two IPC protocols. Hearts were studied ex vivo with regional ischemia (RI) produced by occluding the left anterior descending coronary artery for 30 min followed by 3 h reperfusion. IPC consisted of a 5-min period of global ischemia and either 5 (PC5) or 10 (PC10) min reperfusion before the initiation of index RI. We found that wheel running and PC10, but not PC5, reduced CM death compared with sedentary, with the TRN effect greater in males. TRN, but not IPC, showed functional protection by reducing the loss of left ventricular developed pressure. Surprisingly, the TRN and PC10 protection from cell death was not additive, suggesting that these modalities converge on the same pathway. We also showed that TRN significantly improved mitochondrial respiration and ΔΨ_m repolarization during oxidative phosphorylation after IR when compared with SED rats; the improved bioenergetics was associated with the increased prosurvival kinase, hexokinase II (HKII), translocation to mitochondria, which was mediated by increased total Akt and the phosphorylated Akt. We conclude that TRN-induced cardioprotection is mediated, in part, by preservation of mitochondrial bioenergetics likely mediated via the Akt-pAkt-HKII signaling pathway.<b>NEW & NOTEWORTHY</b> Our study produced the novel findings that wheel running in rats, a form of moderate-intensity continuous training (MICT), can provide protection against IR injury as evidenced by a reduction in cardiomyocyte death following 3 h reperfusion and that the protection generated by MICT and IPC is not additive. Importantly, we demonstrate for the first time that MICT-induced cardioprotection is associated with preservations of mitochondrial bioenergetics likely by the Akt-pAkt-HKII signaling pathway.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1737-C1751"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147872989","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":"Identifying quiescent satellite cells: a scoping review of transcriptomic markers and limitations.","authors":"Anika L Syroid, Alexandra P Steele, Kevin A Murach, Thomas J Hawke","doi":"10.1152/ajpcell.00101.2026","DOIUrl":"10.1152/ajpcell.00101.2026","url":null,"abstract":"<p><p>Skeletal muscle regeneration relies on the resident stem cell population, termed satellite cells. Mechanistically, understanding the quiescence and activation dynamics of muscle satellite cells is essential for regenerative therapies and emerging applications such as cellular agriculture. Quiescent satellite cells (QSCs) are typically identified by expression of paired box 7 (PAX7) and functional characteristics, including a lack of proliferation. However, with the rapidly growing body of transcriptomic data, there is a lack of consensus regarding what markers can be used to identify quiescent satellite cells across transcriptomic studies. The purpose of this review was to evaluate the transcripts currently used to identify QSCs using transcriptomics and to establish an evidence-based foundation that could be used for future analyses. After surveying published single-cell transcriptomic studies, we identified <i>Pax7</i> and/or myogenic factor 5 (<i>Myf5</i>) as the most used markers of general satellite cell identity, whereas sprouty RTK signaling antagonist 1 (<i>Spry1</i>), cluster of differentiation 34 (<i>Cd34</i>), and calcitonin receptor (<i>Calcr</i>), together with the absence of myogenic differentiation 1 (<i>Myod1</i>), marker of proliferation Kiel 67 (<i>Mki67</i>), and cyclin-dependent kinase 1 (<i>Cdk1</i>), were most commonly used to identify QSC clusters in murine studies. In contrast, there is currently insufficient literature to make a confident conclusion on quiescence markers in larger mammals, including humans, pigs, and cattle. We also highlight the conceptual and technical challenges associated with transcriptomic analysis of satellite cell subpopulations, including continuum-based cell states, isolation-induced transcriptional changes, and inconsistent terminology. As a field, greater consistency in language, standardized analyses, and cross-species validation will be required to progress the study of satellite cell quiescence and its translational utility.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1692-C1703"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832333","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":"Fluid shear regulation of local Ca²⁺ transients in right and left rat atrial myocytes under normal and increased beating rate.","authors":"Joon-Chul Kim, Kim Phuong Luong, Sun-Hee Woo","doi":"10.1152/ajpcell.00128.2026","DOIUrl":"10.1152/ajpcell.00128.2026","url":null,"abstract":"<p><p>During volume increase or hemodynamic disturbances in the atrium, fluid shear and beating rate often increase. Shear stress induces Ca²⁺ waves in resting atrial myocytes. Here, we examined whether shear stress alters local Ca²⁺ signaling and how such shear adaptation changes with increased beating frequency in right atrial (RA) and left atrial (LA) myocytes. Using two-dimensional confocal Ca²⁺ imaging in combination with micropuffing, we examined the spatiotemporal properties of junctional (peripheral) and nonjunctional (central) Ca²⁺ signals in field-stimulated rat atrial myocytes. Shear stress (∼16 dyn/cm²) immediately enhanced Ca²⁺ transients, with a larger effect in the center, followed by their inhibition. During the early stimulatory phase only, Ca²⁺ release and decay were prolonged, with greater lengthening in the periphery. Whereas no difference was observed between RA and LA shear responses at 1 Hz, larger stimulatory effects were observed in RA myocytes than LA myocytes at 3 Hz, with no late inhibition. At 3 Hz, only RA myocytes showed early shear-induced prolongation of Ca²⁺ release in the periphery. Sarcoplasmic reticulum (SR) Ca²⁺ contents were similarly reduced by prolonged shear in both sides at 1- and 3-Hz. Increased frequency caused attenuations in Ca²⁺ transients and peripheral SR Ca²⁺ content in LA, but not RA, myocytes under control conditions. Our data suggest that shear stress transiently enhances central Ca²⁺ release during depolarization via prolonged peripheral release but later suppresses it, and that early shear-mediated Ca²⁺ release stimulation deteriorates more readily in LA myocytes at increased frequencies, partly due to a reduced peripheral store.<b>NEW & NOTEWORTHY</b> We demonstrated, for the first time, that shear stress immediately enhances central Ca²⁺ release by prolonging peripheral release during depolarization but suppresses it when sustained. Under increased beating rates, early shear-Ca²⁺ adaptation deteriorates more readily in left than right atrial myocytes due to reduced peripheral Ca²⁺ store. Our data provide a cellular basis for atrial volume- or impinging flow-dependent acute positive inotropy and frequency-dependent differences in its efficiency between right and left atrial myocytes.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1651-C1667"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855507","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 Na⁺/H⁺ exchanger 3 in acidification and morphological remodeling of tubulovesicles in gastric parietal cells.","authors":"Takuto Fujii, Hayato Shimizu, Pattama Wiriyasermkul, Shushi Nagamori, Takahiro Shimizu, Hideki Sakai","doi":"10.1152/ajpcell.00071.2026","DOIUrl":"10.1152/ajpcell.00071.2026","url":null,"abstract":"<p><p>Gastric parietal cells undergo dramatic morphological changes upon stimulation, during which intracellular tubulovesicles (TV) fuse with the apical canalicular membrane to support massive H⁺ secretion by the gastric proton pump (H⁺,K⁺-ATPase). Although the activation process has been extensively characterized, the mechanisms underlying the return to the resting state remain largely unknown. To elucidate this mechanism, we performed proteomic analysis and Western blotting of tubulovesicles isolated from hog stomach. Interestingly, these analyses revealed high expression of the Na⁺/H⁺ exchanger 3 (NHE3) in these tubulovsicles. Immunocytochemical studies further demonstrated colocalization of NHE3 with H⁺,K⁺-ATPase in hog and rat gastric parietal cells. Acridine orange-based measurements of vesicular acidification (H⁺ uptake) in hog tubulovesicles showed that the selective NHE3 inhibitors S3226 and tenapanor significantly enhanced H⁺,K⁺-ATPase-mediated acidification. These inhibitors did not affect the ATPase activity of H⁺,K⁺-ATPase in freeze-dried hog tubulovesicles. This excessive acidification was abolished under Na⁺-free conditions. In addition, ATP-dependent ²²Na⁺ uptake into hog tubulovesicles, which was inhibited by NHE3 inhibitors, was also suppressed by the H⁺,K⁺-ATPase inhibitor SCH28080. In rat primary cultured parietal cells, apical canalicular structures were visualized using an extracellularly applied fluorescent antibody against H⁺,K⁺-ATPase to monitor morphological recovery from the stimulated state (acid-secreting). This analysis revealed that NHE3 inhibitors prevented the transition from the stimulated to the resting state. These findings suggest that NHE3 is functionally coupled with H⁺,K⁺-ATPase in tubulovesicles and may play a critical role in preventing excessive vesicular acidification and facilitating membrane remodeling during the recovery phase.<b>NEW & NOTEWORTHY</b> This study identifies Na⁺/H⁺ exchanger 3 (NHE3) as a key regulator of the transition of gastric parietal cells from the acid-secreting state to the resting state. Using purified gastric tubulovesicles and primary cultured rat parietal cells, we demonstrate for the first time that NHE3 prevents excessive tubulovesicular acidification and promotes membrane remodeling. These findings provide new insight into the homeostasis of parietal cells in the regulation of gastric acid secretion.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1605-C1615"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147653583","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":"Quantitative analysis of skeletal muscle contributions to ECF K⁺ homeostasis.","authors":"Jang H Youn, Stefania Gili, Youngtaek Oh, John Higgins","doi":"10.1152/ajpcell.00160.2026","DOIUrl":"10.1152/ajpcell.00160.2026","url":null,"abstract":"<p><p>There is a division of labor between the kidney and extrarenal tissues in extracellular fluid (ECF) K⁺ homeostasis. The kidney modulates K⁺ excretion to match K⁺ intake, maintaining daily K⁺ balance, whereas extrarenal tissues, primarily skeletal muscle, regulate K⁺ shifts between the ECF and intracellular fluid (ICF). Our recent stable isotope-based modeling study revealed that approximately 98% of the newly administered K⁺ tracer in resting rats was taken up by extrarenal tissues rather than excreted by the kidney within 5 h of administration, indicating that K⁺ exchange between the ECF and ICF pools occurs extremely rapidly. Emerging evidence also suggests that K⁺ influx into skeletal muscle varies linearly with physiological ECF K⁺ concentration ([K⁺]). These characteristics, combined with its large ICF pool, give skeletal muscle both a high capacity for buffering ECF K⁺ and strong control efficiency in modulating K⁺ movements into and out of the ICF. The large K⁺ fluxes into skeletal muscle-and their dependence on ECF [K⁺]-position skeletal muscle as a key regulator of ECF K⁺ homeostasis, alongside insulin, during acute dietary K⁺ intake and in the maintenance of postabsorptive ECF [K⁺]. Furthermore, these features provide a mechanism by which insulin's actions on K⁺ fluxes are attenuated to prevent hypokalemia when a low-K⁺ diet is consumed. In this mini-review, we present quantitative analyses of skeletal muscle function in both acute and long-term K⁺ homeostasis under conditions of altered K⁺ intake, highlighting its role as a sensor, reservoir, and regulator of ECF [K⁺].</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1752-C1759"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13264515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147947532","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":"Forgotten foundations: basement membranes in lung function and cancer.","authors":"Dasol Yoo, Thomas R Cox, Amelia L Parker","doi":"10.1152/ajpcell.00599.2025","DOIUrl":"10.1152/ajpcell.00599.2025","url":null,"abstract":"<p><p>The basement membrane is a specialized extracellular matrix network that orchestrates fundamental cellular processes in many organs. In the lung, this dynamic scaffold provides compositionally encoded instructions that direct epithelial differentiation, regulate injury responses, and modulate disease progression. Despite its fundamental importance, the basement membrane remains an understudied aspect of lung biology, with its precise composition, spatial organization, and biomechanical properties in health and disease poorly defined. This review synthesizes current understanding of lung epithelial basement membrane composition and function with emphasis on how this matrix layer supports lung development, injury repair, and cancer progression. We highlight evidence that basement membrane components are not merely structural supports but active regulators of cellular phenotype and discuss how this conceptual shift opens new therapeutic strategies in lung cancer.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1574-C1593"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147580101","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 double-edged nature of β-catenin: from multicellular innovation to cancer vulnerability.","authors":"Vicente Garrido-Faúndez, Bárbara Castro-Pereira, Clarissa Weil-Echeverría, Fernanda Sandoval-Baeza, Valentina P Sánchez-González, Felipe Robinson, Andrea Ravasio, Gareth I Owen, Cristina Bertocchi","doi":"10.1152/ajpcell.00175.2026","DOIUrl":"10.1152/ajpcell.00175.2026","url":null,"abstract":"<p><p>β-Catenin embodies a fundamental paradox of multicellular life. The same molecular system that enabled the emergence of animal multicellularity by coupling cell-cell adhesion to gene regulation also creates a vulnerability that can drive cancer when misregulated. As a central regulator of cell physiology, β-catenin integrates cell-cell adhesion, mechanotransduction, and gene expression to coordinate tissue architecture with transcriptional programs controlling proliferation, differentiation, and homeostasis. Phylogenomic analyses indicate that bona fide β-catenins form a metazoan-specific monophyletic clade derived from an ancestral armadillo-repeat scaffold. This conserved superhelical structure generates a single interaction groove that mediates mutually exclusive binding to E-cadherin, adenomatous polyposis coli (APC), and T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors. Although this architecture enabled early metazoans to coordinate adhesion, signaling, and morphogenesis, it also introduced an intrinsic regulatory vulnerability. Mutations that disrupt β-catenin degradation stabilize the protein, uncoupling Wnt signaling from its normal regulatory constraints and driving persistent proliferative transcriptional programs. In parallel, emerging structural and biophysical studies reveal conformational plasticity and mechanosensitive properties that enable dynamic partitioning between adhesive and signaling pools. Disruption of these regulatory layers promotes tumor progression, metastasis, immune evasion, and therapy resistance, positioning β-catenin as both a central oncogenic node and a challenging therapeutic target. In this review, we integrate evolutionary, structural, and mechanobiological perspectives to illustrate how β-catenin exemplifies the double-edged nature of biological innovation, an ancient protein that enabled multicellular organization yet whose dysregulation underlies fundamental mechanisms of human cancer.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1760-C1774"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147925600","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":"Sequential invasion assays identify carbonic anhydrase IX as a driver of invasiveness in epithelial triple-negative breast cancer cells.","authors":"Perrin J Black, Destiny D Ball, Alayjha D Edwards, Antonisha R Macintosh, Nobelle I Sakwe, Ngoc B Vuong, Olga Y Korolkova, Vineeta Sharma, Smita Misra, Amos M Sakwe","doi":"10.1152/ajpcell.00088.2026","DOIUrl":"10.1152/ajpcell.00088.2026","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with poor prognosis and diverse response to treatment that is mostly attributed to heterogeneity of the disease that includes a diverse set of tumor cells at various stages of the epithelial-to-mesenchymal transition. Despite advances in our understanding of TNBC biology, isolating the phenotypically distinct cell subpopulations and their molecular drivers of invasiveness remains a major challenge. In this study, we used sequential invasion assays in Boyden chambers coated with growth factor-reduced Matrigel to isolate invasive subpopulations from model migratory mesenchymal-like and proliferative epithelial TNBC cell lines. We ascertained phenotypic heterogeneity of the invasive subpopulations by assessing markers of invasiveness, drug response, growth in three-dimensional cultures, and proteomic analysis. We demonstrated that isolated invasive subpopulations of epithelial cells are E-cadherin-low, whereas those from mesenchymal-like TNBC cells are vimentin-high. The isolated invasive subpopulations are chemotherapy-resistant, stem cell-like cells that express distinct druggable drivers of invasiveness, including carbonic anhydrase 9 (CA9, encoded by the <i>CAIX</i> gene) in the invasive subpopulations of epithelial TNBC cells. Downregulation of <i>CAIX</i> in the invasive subpopulations of epithelial cells resulted in decreased cell proliferation, invasiveness, and sensitivity to chemotherapy. Together, this study demonstrates that targeting specific drivers of invasiveness, such as CA9, in the invasive subpopulations of epithelial cells may provide viable options for novel therapeutic strategies for metastatic TNBC.<b>NEW & NOTEWORTHY</b> This study addressed a major challenge in studying phenotypically distinct cell populations within bulk tumors or cell lines by using sequential invasion assays to reliably isolate vimentin-high mesenchymal-like and E-cadherin-low epithelial invasive subpopulations of TNBC cells. The isolated invasive subpopulations from these phenotypically distinct TNBC cell types are chemotherapy-resistant, stem cell-like, and mammosphere-forming tumor cells that express distinct druggable drivers of invasiveness, including <i>CAIX</i> in the heterogeneous invasive subpopulations of epithelial TNBC cells.</p>","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":" ","pages":"C1616-C1630"},"PeriodicalIF":5.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13262905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147759906","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":"Publisher's note.","authors":"","doi":"10.1152/ajpcell.00197.2026_NOT","DOIUrl":"https://doi.org/10.1152/ajpcell.00197.2026_NOT","url":null,"abstract":"","PeriodicalId":7585,"journal":{"name":"American journal of physiology. Cell physiology","volume":"330 5","pages":"C1559"},"PeriodicalIF":4.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832295","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}