Matrix Biology最新文献

{"title":"Retraction Notice to “RETRACTED: The angiostatic molecule Multimerin 2 is processed by MMP-9 to allow sprouting angiogenesis”","authors":"Eva Andreuzzi , Roberta Colladel , Rosanna Pellicani , Giulia Tarticchio , Renato Cannizzaro , Paola Spessotto , Benedetta Bussolati , Alessia Brossa , Paolo De Paoli , Vincenzo Canzonieri , Renato V. Iozzo , Alfonso Colombatti , Maurizio Mongiat","doi":"10.1016/j.matbio.2025.10.002","DOIUrl":"10.1016/j.matbio.2025.10.002","url":null,"abstract":"","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"142 ","pages":"Pages 86-87"},"PeriodicalIF":4.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145314067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular matrix architecture promotes immunosuppressive microenvironments in pancreatic cancer","authors":"Mackenzie K. Callaway ,&nbsp;Brock J. Noonan ,&nbsp;Kathryn L. Schwertfeger ,&nbsp;Paolo P. Provenzano","doi":"10.1016/j.matbio.2025.09.004","DOIUrl":"10.1016/j.matbio.2025.09.004","url":null,"abstract":"<div><div>Pancreatic ductal adenocarcinoma (PDA) is an aggressive cancer with poor clinical outcomes, due in part to altered fibrotic environments and striking immune dysfunction. Physical properties within tumors, such as aligned extracellular matrix (ECM) fiber architectures, are fundamental to cancer progression and outcome. However, the influence of ECM alignment on immune cell localization and function within tumors, particularly PDA, remains largely unexplored. Here, analysis of mouse and human PDA reveal an inextricable link between collagen architecture and the distribution of immunosuppressive macrophages in both early preinvasive disease and invasive carcinomas. <em>In vitro</em> characterization of primary macrophages demonstrates alignment alone is sufficient to induce elongation, polarization, and immunosuppressive activity, including suppression of CD8+ <em>T</em> cell proliferation and motility. Analysis reveals differential focal adhesion kinase (FAK) activity in aligned macrophages, while FAK inhibition (FAKi) disrupts the immunosuppressive phenotype that emerges from encountering ECM alignment. Furthermore, FAKi <em>in vivo</em> significantly reduces the correlation between elongated immunosuppressive macrophages and aligned collagen, further highlighting the opportunity for FAKi to target stromal immunity. Importantly, the correlation between aligned collagen and immunosuppressive macrophages is also observed in human chronic pancreatitis, a known PDA risk factor that has recently been shown to prime stromal ECM alignments for early dissemination, suggesting that precursor disease is also likely to create stromal memory conducive to early immunosuppression. Taken together, these results support a model in which collagen architecture supports early establishment and maintenance of an immunosuppressive microenvironments and defines a role for targeting stromal matrices to “reprogram” patient immunity.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 114-126"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heparan sulfate N-deacetylase/N-sulfotransferase-1 regulates glioblastoma cell migration and invasion","authors":"Argyris Spyrou ,&nbsp;Ananya Roy ,&nbsp;Anqi Xiong ,&nbsp;Soumi Kundu ,&nbsp;Xi Lu ,&nbsp;Ylva Jansson ,&nbsp;Anna Falk ,&nbsp;Christoph Riethmüller ,&nbsp;Burkhard Greve ,&nbsp;Martin Götte ,&nbsp;Xinqi Chen ,&nbsp;Lena Kjellén ,&nbsp;Karin Forsberg-Nilsson","doi":"10.1016/j.matbio.2025.08.003","DOIUrl":"10.1016/j.matbio.2025.08.003","url":null,"abstract":"<div><div>The glioblastoma (GBM) microenvironment undergoes adaptations to support tumor progression, including a dysregulated extracellular matrix, with altered heparan sulfate (HS) proteoglycans. We investigated N-deacetylase/N-sulfotransferase-1 (NDST1) because NDSTs are initial modifying enzymes of HS biosynthesis and have key roles in designing the HS sulfation pattern. This, in turn governs interactions with growth factors and other biomolecules. We report that NDST1 expression is lower in GBM than in the normal brain, and that patient-derived GBM cells, grown under neural stem cell culture conditions have lower levels of HS than normal astrocytes. Overexpression of NDST1 in GBM cells with low inherent NDST1 levels stimulates cell migration, reduce cell adhesion, induce EMT markers and increase invasion. Conversely, when NDST1 levels were reduced by shRNA in GBM cells, that had higher baseline expression, we find that invasion is reduced, and instead, self-renewal capacity increases alongside elevated stem cell marker expression. Moreover, overexpression of NDST1 changes chromatin accessibility of gene regulatory regions with the capacity to affect transcription factor expression, and pathways that favors cell motility and invasion. Furthermore, NDST1 overexpression results in increased activation of several receptor tyrosine kinases. This study shows that low NDST1 levels support GBM cell stemness, whereas high NDST1 levels endow tumor cells with a motile cell phenotype. We therefore propose that NDST1 is important for regulation of the balance between proliferation and invasive properties in GBM cells.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 1-15"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144838410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomechanical and compositional basement membrane defects due to a Col4a1 mutation affect cardiac morphology and function","authors":"Erin Boland ,&nbsp;Anna Hoyle ,&nbsp;Olivia Robertson-Gray ,&nbsp;William Fuller ,&nbsp;Joe Swift ,&nbsp;Marco Cantini ,&nbsp;Matthew Walker ,&nbsp;Eline Huethorst ,&nbsp;Eilidh MacDonald ,&nbsp;Christoper Loughrey ,&nbsp;Manuel Salmeron-Sanchez ,&nbsp;Godfrey L. Smith ,&nbsp;Fabio Quondamatteo ,&nbsp;Tom Van Agtmael","doi":"10.1016/j.matbio.2025.09.003","DOIUrl":"10.1016/j.matbio.2025.09.003","url":null,"abstract":"<div><div>Collagen IV is a major constituent of basement membranes and mutations in the genes <em>COL4A1</em> and <em>COL4A2</em> present clinically as a variable, multi-system disorder called COL4A1 (Gould) syndrome. Evidence from case reports supports a cardiac component to this disease, but the phenotypic and functional implications affecting the heart, their progression and underlying mechanisms all remain poorly characterised. Indeed, the role of the basement membrane (BM) in adult cardiac disease remains underexplored. We set out to address these knowledge gaps by combining in-depth phenotypic and molecular analyses of a <em>Col4a1</em> mutation on cardiac biology in a murine model (<em>Col4a1^+/svc</em>) of Gould Syndrome. This revealed morphological cardiac defects including cardiomyocyte hypertrophy with myocardial and vascular fibrotic remodelling that impaired cardiac function. The <em>Col4a1</em> mutation causes systolic and diastolic dysfunction with reduced left ventricular developed pressure. Mechanistically, we show these defects are due to secretion of mutant protein and BM defects rather than collagen misfolding and proteotoxic stress. The BM defects lead to a pro-fibrotic state with increased fibrillar collagen deposition, cardiac stiffness, and ECM compositional defects. These are accompanied by altered regulation of pathways involved in sarcomere formation, sarcolemma stability and cardiomyocyte metabolism, establishing a molecular signature of COL4A1-related cardiac disease. Intriguingly, aspects of this molecular signature including cardiac metabolic pathways, regulation of cardiac muscle contraction and BM component expression, are shared with common cardiomyopathies such as coronary micro-embolism, and dilated, ischemic and hypertrophic obstructive cardiomyopathies. By defining the molecular and phenotypic cardiac components of Gould syndrome these data show that the BM is essential for maintaining systolic and diastolic function and that alterations to the BM leads to a fibrotic response. These data increase insight into the role of the basement membrane and collagen IV in cardiac biology, and highlights mechanisms shared between Gould syndrome and common adult cardiac disease.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 82-100"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Decorin deficiency promotes epithelial-mesenchymal transition and colon cancer metastasis” [Matrix Biology Volume 95 (2021)1-14]","authors":"Liping Mao ,&nbsp;Jinxue Yang ,&nbsp;Jiaxin Yue ,&nbsp;Yang Chen ,&nbsp;Hongrui Zhou ,&nbsp;Dongdong Fan ,&nbsp;Qiuhua Zhang ,&nbsp;Simone Buraschi ,&nbsp;Renato V. Iozzo ,&nbsp;Xiuli Bi","doi":"10.1016/j.matbio.2025.08.002","DOIUrl":"10.1016/j.matbio.2025.08.002","url":null,"abstract":"","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Page 127"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144876416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence for the major role of PH4⍺EFB in the prolyl 4-hydroxylation of Drosophila collagen IV","authors":"Yoshihiro Ishikawa ,&nbsp;Melissa A. Toups ,&nbsp;Marwan Elkrewi ,&nbsp;Allison L. Zajac ,&nbsp;Sally Horne-Badovinac ,&nbsp;Yutaka Matsubayashi","doi":"10.1016/j.matbio.2025.09.002","DOIUrl":"10.1016/j.matbio.2025.09.002","url":null,"abstract":"<div><div>Collagens are fundamental components of extracellular matrices, requiring precise intracellular post-translational modifications for proper function. Among the modifications, prolyl 4-hydroxylation is critical to stabilise the collagen triple helix. In humans, this reaction is mediated by collagen prolyl 4-hydroxylases (P4Hs). While humans possess three genes encoding these enzymes (P4H⍺s), <em>Drosophila melanogaster</em> harbour at least 26 candidates for collagen P4H⍺s despite its simple genome, and it is poorly understood which of them are actually working on collagen in the fly. In this study, we addressed this question by carrying out thorough bioinformatic and biochemical analyses. We demonstrate that among the 26 potential collagen P4H⍺s, PH4⍺EFB shares the highest homology with vertebrate collagen P4H⍺s. Furthermore, while collagen P4Hs and their substrates must exist in the same cells, our transcriptomic analyses at the tissue and single cell levels showed a global co-expression of <em>PH4⍺EFB</em> but not the other P4H⍺-related genes with the collagen IV genes. Moreover, expression of <em>PH4⍺EFB</em> during embryogenesis was found to precede that of collagen IV, presumably enabling efficient collagen modification by PH4⍺EFB. Finally, biochemical assays confirm that PH4⍺EFB binds collagen, supporting its direct role in collagen IV modification. Collectively, we identify PH4⍺EFB as the primary and potentially constitutive prolyl 4-hydroxylase responsible for collagen IV biosynthesis in <em>Drosophila</em>. Our findings highlight the remarkably simple nature of <em>Drosophila</em> collagen IV biosynthesis, which may serve as a blueprint for defining the minimal requirements for collagen engineering.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 101-113"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145066249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring basement membrane dynamics through cross-scale imaging, manipulation, and molecular mapping","authors":"Kohei Omachi,&nbsp;Hironobu Fujiwara","doi":"10.1016/j.matbio.2025.09.001","DOIUrl":"10.1016/j.matbio.2025.09.001","url":null,"abstract":"<div><div>The basement membrane (BM), a specialized extracellular matrix (ECM), provides structural support for epithelial, endothelial, and other parenchymal cells. Once considered a static scaffold, the BM is now recognized as a dynamic and complex nanostructure composed of a diversity of molecules that actively regulate cell behavior and tissue organization. Its molecular composition, assembly, and remodeling are precisely controlled in a tissue- and stage-specific manner, contributing to the regulation of local and global mechanical properties and biochemical signaling. Understanding BM structure and function requires integrated approaches across biological scales—from nanoscale molecular interactions to tissue-level architecture. In this review, we highlight advances in three methodological areas: (1) imaging techniques that reveal BM nanostructure and dynamics, (2) manipulation strategies that uncover causal roles of BM components, and (3) omics-based approaches that map BM composition and cellular sources. Integrating these strategies enables the bridging of molecular events and organ-level functions, offering new insights into how the BM is involved in development, homeostasis, and disease progression. The aim of this review is to provide researchers with a comprehensive perspective on evolving tools for dissecting BM structure, dynamics, and function.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 67-81"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145001856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Laminin γ1 chain is essential for the cardiorespiratory and muscular systems","authors":"Kinga I. Gawlik ,&nbsp;Deniz A. Bölükbas ,&nbsp;Fatima Daoud ,&nbsp;Niccolò Peruzzi ,&nbsp;Ellinor Welinder ,&nbsp;Trevor S. Wendt ,&nbsp;Marycarmen Arévalo Martinez ,&nbsp;Sinem Tas ,&nbsp;Johan Holmberg ,&nbsp;Nika Gvazava ,&nbsp;Saema Ansar ,&nbsp;Sebastian Albinsson ,&nbsp;Darcy Wagner ,&nbsp;Karl Swärd ,&nbsp;Karin Tran-Lundmark ,&nbsp;Madeleine Durbeej","doi":"10.1016/j.matbio.2025.08.006","DOIUrl":"10.1016/j.matbio.2025.08.006","url":null,"abstract":"<div><div>Laminins are basement membrane components that regulate a plethora of biological processes. Despite decades of research, the exact roles of laminins in different tissues and in organogenesis remain to be elucidated. Here, we investigated the function of laminin γ1 chain in heart, lung and other tissues by generating a mouse that lacks laminin γ1 in cells expressing SM22α (<em>Tagln</em>) (LMγ1 flox/SM22α Cre mouse, referred to as LMγ1KO). Laminin γ1 deletion led to basement membrane disruption around cardiomyocytes, smooth muscle cells, alveolar cells and skeletal muscle. This, in turn, led to perinatal death of conditional LMγ1KO mice. Synchrotron-based imaging revealed developmental heart abnormalities: ventricular and atrioventricular septal defects. Lung tissue from embryos and newborns showed impaired alveolization and this defect was not reversed <em>ex vivo</em>. We also created adult inducible laminin γ1 knockout mice (iLMγ1KO) with targeted knockdown in all tissues, and they exhibited decreased contractility of smooth muscle in colonic and arterial tissue. Finally, both LMγ1KO neonates and iLMγ1KO adults displayed severe dystrophic features in skeletal muscle.</div><div>In summary, our study reveals novel roles for laminin γ1 chain and basement membranes in heart, lung, skeletal and smooth muscle. Compromising basement membranes around various cell types expressing SM22α during embryonic development did not impair early organogenesis of lung, heart and skeletal muscle, but rather disturbed late developmental events in these tissues. Our results could help to understand clinical implications for patients with laminin α2 chain mutations (muscular dystrophy) and laminin α4 mutations (cardiomyopathy), but also for patients with congenital heart disease and lung diseases.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 47-66"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Basement membrane structure and function: Relating biology to mechanics","authors":"Andrea Page-McCaw ,&nbsp;Nicholas Ferrell","doi":"10.1016/j.matbio.2025.08.004","DOIUrl":"10.1016/j.matbio.2025.08.004","url":null,"abstract":"<div><div>Basement membranes are key mediators of many biological processes such as epithelial morphogenesis, kidney filtration, and muscle function among others. Basement membranes provide structural support to tissues so understanding their mechanical properties is important for determining how they contribute to tissue form and function. Further, basement membranes are altered in many diseases including cancer, diabetes, and fibrosis, and these changes may contribute to disease pathogenesis and progression. Understanding how basement membrane mechanics integrate with tissue function is the work of both biologists and engineers/material scientists, yet these disciplines have very different foundations. This review discusses basement membrane macromolecular structure with a view to illuminate how this structure confers basement membranes with unique mechanical properties adapted to resisting physiological stresses. The pathological implications of altered basement membrane mechanics are discussed in the context of different diseases. Additionally, we survey methods used to measure basement membrane mechanical properties, including atomic force microscopy, tensile stiffness assays, and non-quantitative assays such as cell bursting, assessing their strengths and limitations and their accessibility for different types of <em>in vivo</em> studies. We focus on explaining and illuminating the complexities of basement membrane material properties for biologists, and explaining the biological aspects for engineers, with the goal of making interdisciplinary science more accessible to experimentalists and readers.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 16-31"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of col4a1 in zebrafish recapitulates the cerebrovascular phenotypes associated with monogenic cerebral small vessel disease","authors":"Daisy Flatman ,&nbsp;Richard W Naylor ,&nbsp;Siobhan Crilly ,&nbsp;Isabel Carter ,&nbsp;Aleksandr Mironov ,&nbsp;Emmanuel Pinteaux ,&nbsp;Stuart M. Allan ,&nbsp;Rachel Lennon ,&nbsp;Paul R. Kasher","doi":"10.1016/j.matbio.2025.08.005","DOIUrl":"10.1016/j.matbio.2025.08.005","url":null,"abstract":"<div><div>Cerebral small vessel disease (cSVD) is a major cause of vascular dementia and stroke. Our understanding of cSVD pathophysiology is incomplete and our ability to treat patients is limited. Pathogenic variants in type IV collagen alpha 1 (<em>COL4A1</em>) cause a monogenic form of cSVD with variable age of onset, via disturbance of cerebrovascular basement membranes. Zebrafish larvae are a powerful model organism for studying cerebrovascular disease due to their optical clarity and applicability for live imaging. In this study, we characterised a zebrafish crispant model for loss-of-function <em>COL4A1</em>-associated cSVD that successfully recapitulates key disease features, including spontaneous intracerebral haemorrhage and cerebrovascular abnormalities. We also identified evidence for abnormal cerebrovascular basement membranes and elevated matrix metalloproteinase 9 (<em>mmp9)</em> transcription associated with loss of <em>col4a1</em>. Pharmacological inhibition of mmp9 was sufficient to ameliorate some cerebrovascular phenotypes. Finally, we describe the generation of a mutant line carrying a germline-transmissible 20 bp deletion in zebrafish <em>col4a1</em> (<em>col4a1</em>^Δ20) which is associated with cerebrovascular abnormalities, swimming defects and increased susceptibility to pharmacologically induced brain haemorrhages during larval stages. In adulthood, mutant <em>col4a1</em>^Δ20 animals developed spontaneous brain haemorrhages that were observable in free-swimming fish. Overall, this study validates the use of zebrafish disease modelling for preclinical <em>COL4A1</em>-associated cSVD research and highlights its potential for further understanding disease pathophysiology and future drug discovery projects.</div></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"141 ","pages":"Pages 32-46"},"PeriodicalIF":4.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144900307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}