Matrix Biology最新文献_第9页

LPA-induced expression of CCN2 in muscular fibro/adipogenic progenitors (FAPs): Unraveling cellular communication networks LPA 诱导的 CCN2 在肌肉纤维/脂肪生成原（FAPs）中的表达：揭示细胞通讯网络。

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-05-07 DOI: 10.1016/j.matbio.2024.05.001

Adriana Córdova-Casanova , Meilyn Cruz-Soca , Felipe S. Gallardo , Jennifer Faundez-Contreras , Alexia Bock-Pereda , Jerold Chun , Carlos P. Vio , Juan Carlos Casar , Enrique Brandan

{"title":"LPA-induced expression of CCN2 in muscular fibro/adipogenic progenitors (FAPs): Unraveling cellular communication networks","authors":"Adriana Córdova-Casanova , Meilyn Cruz-Soca , Felipe S. Gallardo , Jennifer Faundez-Contreras , Alexia Bock-Pereda , Jerold Chun , Carlos P. Vio , Juan Carlos Casar , Enrique Brandan","doi":"10.1016/j.matbio.2024.05.001","DOIUrl":"10.1016/j.matbio.2024.05.001","url":null,"abstract":"<div><p>Cellular Communication Network Factor 2, CCN2, is a profibrotic cytokine implicated in physiological and pathological processes in mammals. The expression of CCN2 is markedly increased in dystrophic muscles. Interestingly, diminishing CCN2 genetically or inhibiting its function improves the phenotypes of chronic muscular fibrosis in rodent models. Elucidating the cell-specific mechanisms behind the induction of CCN2 is a fundamental step in understanding its relevance in muscular dystrophies. Here, we show that the small lipids LPA and 2S-OMPT induce CCN2 expression in fibro/adipogenic progenitors (FAPs) through the activation of the LPA<sub>1</sub> receptor and, to a lower extent, by also the LPA<sub>6</sub> receptor. These cells show a stronger induction than myoblasts or myotubes. We show that the LPA/LPARs axis requires ROCK kinase activity and organized actin cytoskeleton upstream of YAP/TAZ signaling effectors to upregulate CCN2 levels, suggesting that mechanical signals are part of the mechanism behind this process. In conclusion, we explored the role of the LPA/LPAR axis on CCN2 expression, showing a strong cytoskeletal-dependent response in muscular FAPs.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"130 ","pages":"Pages 36-46"},"PeriodicalIF":6.9,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899651","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}

引用次数: 0

Transglutaminase-mediated stiffening of the glomerular basement membrane mitigates pressure-induced reductions in molecular sieving coefficient by reducing compression 由转谷氨酰胺酶介导的肾小球基底膜硬化可通过减少压缩减轻压力引起的分子筛分系数降低。

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-05-07 DOI: 10.1016/j.matbio.2024.05.002

Dan Wang, Nicholas Ferrell

{"title":"Transglutaminase-mediated stiffening of the glomerular basement membrane mitigates pressure-induced reductions in molecular sieving coefficient by reducing compression","authors":"Dan Wang, Nicholas Ferrell","doi":"10.1016/j.matbio.2024.05.002","DOIUrl":"10.1016/j.matbio.2024.05.002","url":null,"abstract":"<div><p>Proteinuria, the presence of high molecular weight proteins in the urine, is a primary indicator of chronic kidney disease. Proteinuria results from increased molecular permeability of the glomerular filtration barrier combined with saturation or defects in tubular protein reabsorption. Any solute that passes into the glomerular filtrate traverses the glomerular endothelium, the glomerular basement membrane, and the podocyte slit diaphragm. Damage to any layer of the filter has reciprocal effects on other layers to increase glomerular permeability. The GBM is thought to act as a compressible ultrafilter that has increased molecular selectivity with increased pressure due to compression that reduced the porosity of the GBM with increased pressure. In multiple forms of chronic kidney disease, crosslinking enzymes are upregulated and may act to increase GBM stiffness. Here we show that enzymatically crosslinking porcine GBM with transglutaminase increases the stiffness of the GBM and mitigates pressure-dependent reductions in molecular sieving coefficient. This was modeled mathematically using a modified membrane transport model accounting for GBM compression. Changes in the mechanical properties of the GBM may contribute to proteinuria through pressure-dependent effects on GBM porosity.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"130 ","pages":"Pages 47-55"},"PeriodicalIF":6.9,"publicationDate":"2024-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000635/pdfft?md5=ca3c58b7bcee7290a259da192b79305e&pid=1-s2.0-S0945053X24000635-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140899656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to “Fibrolamellar carcinomas–growth arrested by paracrine signals complexed with synthesized 3-O sulfated heparan sulfate oligosaccharides” [Matrix Biology 121(August 2023), 194–216] 纤维母细胞癌--与合成的 3-O 硫酸化硫酸肝素低聚糖复合的旁分泌信号抑制了生长》[《基质生物学》121（2023 年 8 月），194-216] 更正

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-05-01 DOI: 10.1016/j.matbio.2024.03.004

Wencheng Zhang , Yongmei Xu , Xicheng Wang , Tsunekazu Oikawa , Guowei Su , Eliane Wauthier , Guoxiu Wu , Praveen Sethupathy , Zhiying He , Jian Liu , Lola M. Reid

引用次数: 0

Integrating integrins with the hallmarks of cancer 将整合素与癌症特征相结合

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-04-25 DOI: 10.1016/j.matbio.2024.04.003

Scott M. Haake , Brenda L. Rios , Ambra Pozzi , Roy Zent

{"title":"Integrating integrins with the hallmarks of cancer","authors":"Scott M. Haake , Brenda L. Rios , Ambra Pozzi , Roy Zent","doi":"10.1016/j.matbio.2024.04.003","DOIUrl":"10.1016/j.matbio.2024.04.003","url":null,"abstract":"<div><p>Epithelial cells adhere to a specialized extracellular matrix called the basement membrane which allows them to polarize and form epithelial tissues. The extracellular matrix provides essential physical scaffolding and biochemical and biophysical cues required for tissue morphogenesis, differentiation, function, and homeostasis. Epithelial cell adhesion to the extracellular matrix (i.e., basement membrane) plays a critical role in organizing epithelial tissues, separating the epithelial cells from the stroma. Epithelial cell detachment from the basement membrane classically results in death, though detachment or invasion through the basement membrane represents a critical step in carcinogenesis. Epithelial cells bind to the extracellular matrix via specialized matrix receptors, including integrins. Integrins are transmembrane receptors that form a mechanical linkage between the extracellular matrix and the intracellular cytoskeleton and are required for anchorage-dependent cellular functions such as proliferation, migration, and invasion. The role of integrins in the development, growth, and dissemination of multiple types of carcinomas has been investigated by numerous methodologies, which has led to great complexity. To organize this vast array of information, we have utilized the “Hallmarks of Cancer” from Hanahan and Weinberg as a convenient framework to discuss the role of integrins in the pathogenesis of cancers. This review explores this biology and how its complexity has impacted the development of integrin-targeted anti-cancer therapeutics.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"130 ","pages":"Pages 20-35"},"PeriodicalIF":6.9,"publicationDate":"2024-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000532/pdfft?md5=7db7381a2479c463e647a0fbb117f855&pid=1-s2.0-S0945053X24000532-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140794527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tenascin-C targeting strategies in cancer 癌症中的 Tenascin-C 靶向策略

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-04-18 DOI: 10.1016/j.matbio.2024.04.002

Sayda Dhaouadi , Balkiss Bouhaouala-Zahar , Gertraud Orend

引用次数: 0

The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy 在不同形式的肌肉萎缩症中，细胞外基质对肌母细胞的运动和分化具有不同的指导作用：肌营养不良性基质改变了肌母细胞的运动能力

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-04-04 DOI: 10.1016/j.matbio.2024.04.001

Ashlee M. Long , Jason M. Kwon , GaHyun Lee , Nina L. Reiser , Lauren A. Vaught , Joseph G. O'Brien , Patrick G.T. Page , Michele Hadhazy , Joseph C. Reynolds , Rachelle H. Crosbie , Alexis R. Demonbreun , Elizabeth M. McNally

{"title":"The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy","authors":"Ashlee M. Long , Jason M. Kwon , GaHyun Lee , Nina L. Reiser , Lauren A. Vaught , Joseph G. O'Brien , Patrick G.T. Page , Michele Hadhazy , Joseph C. Reynolds , Rachelle H. Crosbie , Alexis R. Demonbreun , Elizabeth M. McNally","doi":"10.1016/j.matbio.2024.04.001","DOIUrl":"10.1016/j.matbio.2024.04.001","url":null,"abstract":"<div><p>Extracellular matrix (ECM) pathologic remodeling underlies many disorders, including muscular dystrophy. Tissue decellularization removes cellular components while leaving behind ECM components. We generated “on-slide” decellularized tissue slices from genetically distinct dystrophic mouse models. The ECM of dystrophin- and sarcoglycan-deficient muscles had marked thrombospondin 4 deposition, while dysferlin-deficient muscle had excess decorin. Annexins A2 and A6 were present on all dystrophic decellularized ECMs, but annexin matrix deposition was excessive in dysferlin-deficient muscular dystrophy. Muscle-directed viral expression of annexin A6 resulted in annexin A6 in the ECM. C2C12 myoblasts seeded onto decellularized matrices displayed differential myoblast mobility and fusion. Dystrophin-deficient decellularized matrices inhibited myoblast mobility, while dysferlin-deficient decellularized matrices enhanced myoblast movement and differentiation. Myoblasts treated with recombinant annexin A6 increased mobility and fusion like that seen on dysferlin-deficient decellularized matrix and demonstrated upregulation of ECM and muscle cell differentiation genes. These findings demonstrate specific fibrotic signatures elicit effects on myoblast activity.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"129 ","pages":"Pages 44-58"},"PeriodicalIF":6.9,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140542219","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}

引用次数: 0

Heparan sulfate selectively inhibits the collagenase activity of cathepsin K 硫酸头孢选择性地抑制 cathepsin K 的胶原酶活性。

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-03-26 DOI: 10.1016/j.matbio.2024.03.005

Xiaoxiao Zhang , Yin Luo , Huanmeng Hao , Juno M. Krahn , Guowei Su , Robert Dutcher , Yongmei Xu , Jian Liu , Lars C. Pedersen , Ding Xu

{"title":"Heparan sulfate selectively inhibits the collagenase activity of cathepsin K","authors":"Xiaoxiao Zhang , Yin Luo , Huanmeng Hao , Juno M. Krahn , Guowei Su , Robert Dutcher , Yongmei Xu , Jian Liu , Lars C. Pedersen , Ding Xu","doi":"10.1016/j.matbio.2024.03.005","DOIUrl":"10.1016/j.matbio.2024.03.005","url":null,"abstract":"<div><p>Cathepsin K (CtsK) is a cysteine protease with potent collagenase activity. CtsK is highly expressed by bone-resorbing osteoclasts and plays an essential role in resorption of bone matrix. Although CtsK is known to bind heparan sulfate (HS), the structural details of the interaction, and how HS regulates the biological functions of CtsK, remains largely unknown. In this report, we discovered that HS is a multifaceted regulator of the structure and function of CtsK. Structurally, HS forms a highly stable complex with CtsK and induces its dimerization. Co-crystal structures of CtsK with bound HS oligosaccharides reveal the location of the HS binding site and suggest how HS may support dimerization. Functionally, HS plays a dual role in regulating the enzymatic activity of CtsK. While it preserves the peptidase activity of CtsK by stabilizing its active conformation, it inhibits the collagenase activity of CtsK in a sulfation level-dependent manner. These opposing effects can be explained by our finding that the HS binding site is remote from the active site, which allows HS to specifically inhibit the collagenase activity without affecting the peptidase activity. At last, we show that structurally defined HS oligosaccharides effectively block osteoclast resorption of bone <em>in vitro</em> without inhibiting osteoclast differentiation, which suggests that HS-based oligosaccharide might be explored as a new class of selective CtsK inhibitor for many diseases involving exaggerated bone resorption.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"129 ","pages":"Pages 15-28"},"PeriodicalIF":6.9,"publicationDate":"2024-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140319646","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}

引用次数: 0

AβPP-tau-HAS1 axis trigger HAS1-related nuclear speckles and gene transcription in Alzheimer's disease AβPP-tau-HAS1 轴触发阿尔茨海默病中与 HAS1 相关的核斑点和基因转录。

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-03-20 DOI: 10.1016/j.matbio.2024.03.003

Ya-Hong Zhang , Xing-Tong Sun , Rui-Fang Guo , Gang-Yi Feng , Hui-Ling Gao , Man-Li Zhong , Li-Wen Tian , Zhong-Yi Qiu , Yu-Wei Cui , Jia-Yi Li , Pu Zhao

{"title":"AβPP-tau-HAS1 axis trigger HAS1-related nuclear speckles and gene transcription in Alzheimer's disease","authors":"Ya-Hong Zhang , Xing-Tong Sun , Rui-Fang Guo , Gang-Yi Feng , Hui-Ling Gao , Man-Li Zhong , Li-Wen Tian , Zhong-Yi Qiu , Yu-Wei Cui , Jia-Yi Li , Pu Zhao","doi":"10.1016/j.matbio.2024.03.003","DOIUrl":"10.1016/j.matbio.2024.03.003","url":null,"abstract":"<div><p>As the backbone of the extracellular matrix (ECM) and the perineuronal nets (PNNs), hyaluronic acid (HA) provides binding sites for proteoglycans and other ECM components. Although the pivotal of HA has been recognized in Alzheimer's disease (AD), few studies have addressed the relationship between AD pathology and HA synthases (HASs). Here, HASs in different regions of AD brains were screened in transcriptomic database and validated in AβPP/PS1 mice. We found that HAS1 was distributed along the axon and nucleus. Its transcripts were reduced in AD patients and AβPP/PS1 mice. Phosphorylated tau (p-tau) mediates AβPP-induced cytosolic-nuclear translocation of HAS1, and negatively regulated the stability, monoubiquitination, and oligomerization of HAS1, thus reduced the synthesis and release of HA. Furthermore, non-ubiquitinated HAS1 mutant lost its enzyme activity, and translocated from the cytosol into the nucleus, forming nuclear speckles (NS). Unlike the splicing-related NS, less than 1 % of the non-ubiquitinated HAS1 co-localized with SRRM2, proving the regulatory role of HAS1 in gene transcription, indirectly. Thus, differentially expressed genes (DEGs) related to both non-ubiquitinated HAS1 mutant and AD were screened using transcriptomic datasets. Thirty-nine DEGs were identified, with 64.1 % (25/39) showing consistent results in both datasets. Together, we unearthed an important function of the AβPP-p-tau-HAS1 axis in microenvironment remodeling and gene transcription during AD progression, involving the ubiquitin-proteasome, lysosome, and NS systems.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"129 ","pages":"Pages 29-43"},"PeriodicalIF":6.9,"publicationDate":"2024-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140190338","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}

引用次数: 0

Hyaluronan degradation by HYAL2 is essential for odontoblastic differentiation and migration of mouse dental papilla cells HYAL2降解透明质酸对小鼠牙乳头细胞的牙骨质分化和迁移至关重要。

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-03-13 DOI: 10.1016/j.matbio.2024.03.002

Haiyan Huang , Xiaoyu Hu , Jiayan Wu , Chenyu Song , Zhixin Tian , Beizhan Jiang

{"title":"Hyaluronan degradation by HYAL2 is essential for odontoblastic differentiation and migration of mouse dental papilla cells","authors":"Haiyan Huang , Xiaoyu Hu , Jiayan Wu , Chenyu Song , Zhixin Tian , Beizhan Jiang","doi":"10.1016/j.matbio.2024.03.002","DOIUrl":"10.1016/j.matbio.2024.03.002","url":null,"abstract":"<div><p>The coordination between odontoblastic differentiation and directed cell migration of mesenchymal progenitors is necessary for regular dentin formation. The synthesis and degradation of hyaluronan (HA) in the extracellular matrix create a permissive niche that directly regulates cell behaviors. However, the role and mechanisms of HA degradation in dentin formation remain unknown. In this work, we present that HA digestion promotes odontoblastic differentiation and cell migration of mouse dental papilla cells (mDPCs). Hyaluronidase 2 (HYAL2) is responsible for promoting odontoblastic differentiation through degrading HA, while hyaluronidase 1 (HYAL1) exhibits negligible effect. Silencing <em>Hyal2</em> generates an extracellular environment rich in HA, which attenuates F-actin and filopodium formation and in turn inhibits cell migration of mDPCs. In addition, activating PI3K/Akt signaling significantly rescues the effects of HA accumulation on cytodifferentiation. Taken together, the results confirm the contribution of HYAL2 to HA degradation in dentinogenesis and uncover the mechanism of the HYAL2-mediated HA degradation in regulating the odontoblastic differentiation and migration of mDPCs.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"129 ","pages":"Pages 1-14"},"PeriodicalIF":6.9,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140137338","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}

引用次数: 0

Macrophage phenotype is determinant for fibrosis development in keloid disease 巨噬细胞表型是瘢痕疙瘩病纤维化发展的决定因素

IF 6.9 1区生物学

Matrix Biology Pub Date : 2024-03-12 DOI: 10.1016/j.matbio.2024.03.001

Zélie Dirand , Mélissa Maraux , Marion Tissot , Brice Chatelain , Dorothy Supp , Céline Viennet , Sylvain Perruche , Gwenaël Rolin

{"title":"Macrophage phenotype is determinant for fibrosis development in keloid disease","authors":"Zélie Dirand , Mélissa Maraux , Marion Tissot , Brice Chatelain , Dorothy Supp , Céline Viennet , Sylvain Perruche , Gwenaël Rolin","doi":"10.1016/j.matbio.2024.03.001","DOIUrl":"10.1016/j.matbio.2024.03.001","url":null,"abstract":"<div><p>Keloid refers to a fibroproliferative disorder characterized by an accumulation of extracellular matrix (ECM) components at the dermis level, overgrowth beyond initial wound, and formation of tumor-like nodule areas. Treating keloid is still an unmet clinical need and the lack of an efficient therapy is clearly related to limited knowledge about keloid etiology, despite the growing interest of the scientific community in this pathology. In past decades, keloids were often studied <em>in vitro</em> through the sole prism of fibroblasts considered as the major effector of ECM deposition. Nevertheless, development of keloids results from cross-interactions of keloid fibroblasts (KFs) and their surrounding microenvironment, including immune cells such as macrophages. Our study aimed to evaluate the effect of M1 and M2 monocyte-derived macrophages on KFs <em>in vitro</em>. We focused on the effects of the macrophage secretome on fibrosis-related criteria in KFs, including proliferation, migration, differentiation, and ECM synthesis. First, we demonstrated that M2-like macrophages enhanced the fibrogenic profile of KFs in culture. Then, we surprisingly founded that M1-like macrophages can have an anti-fibrogenic effect on KFs, even in a pro-fibrotic environment. These results demonstrate, for the first time, that M1 and M2 macrophage subsets differentially impact the fibrotic fate of KFs <em>in vitro</em>, and suggest that restoring the M1/M2 balance to favor M1 in keloids could be an efficient therapeutic lever to prevent or treat keloid fibrosis.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"128 ","pages":"Pages 79-92"},"PeriodicalIF":6.9,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000374/pdfft?md5=2493e18800441c6bd0e5a5340b3f35ff&pid=1-s2.0-S0945053X24000374-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140117702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0