Matrix Biology最新文献

{"title":"Integrating integrins with the hallmarks of cancer","authors":"Scott M. Haake ,&nbsp;Brenda L. Rios ,&nbsp;Ambra Pozzi ,&nbsp;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}

{"title":"Tenascin-C targeting strategies in cancer","authors":"Sayda Dhaouadi ,&nbsp;Balkiss Bouhaouala-Zahar ,&nbsp;Gertraud Orend","doi":"10.1016/j.matbio.2024.04.002","DOIUrl":"https://doi.org/10.1016/j.matbio.2024.04.002","url":null,"abstract":"<div><p>Tenascin-C (TNC) is a matricellular and multimodular glycoprotein highly expressed under pathological conditions, especially in cancer and chronic inflammatory diseases. Since a long time TNC is considered as a promising target for diagnostic and therapeutic approaches in anti-cancer treatments and was already extensively targeted in clinical trials on cancer patients. This review provides an overview of the current most advanced strategies used for TNC detection and anti-TNC theranostic approaches including some advanced clinical strategies. We also discuss novel treatment protocols, where targeting immune modulating functions of TNC could be center stage.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"130 ","pages":"Pages 1-19"},"PeriodicalIF":6.9,"publicationDate":"2024-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140647681","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":"The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy","authors":"Ashlee M. Long ,&nbsp;Jason M. Kwon ,&nbsp;GaHyun Lee ,&nbsp;Nina L. Reiser ,&nbsp;Lauren A. Vaught ,&nbsp;Joseph G. O'Brien ,&nbsp;Patrick G.T. Page ,&nbsp;Michele Hadhazy ,&nbsp;Joseph C. Reynolds ,&nbsp;Rachelle H. Crosbie ,&nbsp;Alexis R. Demonbreun ,&nbsp;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}

{"title":"Heparan sulfate selectively inhibits the collagenase activity of cathepsin K","authors":"Xiaoxiao Zhang ,&nbsp;Yin Luo ,&nbsp;Huanmeng Hao ,&nbsp;Juno M. Krahn ,&nbsp;Guowei Su ,&nbsp;Robert Dutcher ,&nbsp;Yongmei Xu ,&nbsp;Jian Liu ,&nbsp;Lars C. Pedersen ,&nbsp;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}

{"title":"AβPP-tau-HAS1 axis trigger HAS1-related nuclear speckles and gene transcription in Alzheimer's disease","authors":"Ya-Hong Zhang ,&nbsp;Xing-Tong Sun ,&nbsp;Rui-Fang Guo ,&nbsp;Gang-Yi Feng ,&nbsp;Hui-Ling Gao ,&nbsp;Man-Li Zhong ,&nbsp;Li-Wen Tian ,&nbsp;Zhong-Yi Qiu ,&nbsp;Yu-Wei Cui ,&nbsp;Jia-Yi Li ,&nbsp;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}

{"title":"Hyaluronan degradation by HYAL2 is essential for odontoblastic differentiation and migration of mouse dental papilla cells","authors":"Haiyan Huang ,&nbsp;Xiaoyu Hu ,&nbsp;Jiayan Wu ,&nbsp;Chenyu Song ,&nbsp;Zhixin Tian ,&nbsp;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}

{"title":"Macrophage phenotype is determinant for fibrosis development in keloid disease","authors":"Zélie Dirand ,&nbsp;Mélissa Maraux ,&nbsp;Marion Tissot ,&nbsp;Brice Chatelain ,&nbsp;Dorothy Supp ,&nbsp;Céline Viennet ,&nbsp;Sylvain Perruche ,&nbsp;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}

{"title":"The role of fibrosis in cardiomyopathies: An opportunity to develop novel biomarkers of disease activity","authors":"Elisavet Angeli ,&nbsp;Maria Jordan ,&nbsp;Mandy Otto ,&nbsp;Stevan D. Stojanović ,&nbsp;Morten Karsdal ,&nbsp;Johann Bauersachs ,&nbsp;Thomas Thum ,&nbsp;Jan Fiedler ,&nbsp;Federica Genovese","doi":"10.1016/j.matbio.2024.02.008","DOIUrl":"10.1016/j.matbio.2024.02.008","url":null,"abstract":"<div><p>Cardiomyopathies encompass a spectrum of heart disorders with diverse causes and presentations. Fibrosis stands out as a shared hallmark among various cardiomyopathies, reflecting a common thread in their pathogenesis. This prevalent fibrotic response is intricately linked to the consequences of dysregulated extracellular matrix (ECM) remodeling, emphasizing its significance in the development and progression the disease. This review explores the ECM involvement in various cardiomyopathies and its impact on myocardial stiffness and fibrosis. Additionally, we discuss the potential of ECM fragments as early diagnosis, prognosis, and risk stratification. Biomarkers deriving from turnover of collagens and other ECM proteins hold promise in clinical applications. We outline current clinical management, future directions, and the potential for personalized ECM-targeted therapies with specific focus on microRNAs. In summary, this review examines the role of the fibrosis in cardiomyopathies, highlighting the potential of ECM-derived biomarkers in improving disease management with implications for precision medicine.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"128 ","pages":"Pages 65-78"},"PeriodicalIF":6.9,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139998106","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":"The role of positional information in determining dermal fibroblast diversity","authors":"Pratyusha Chitturi,&nbsp;Andrew Leask","doi":"10.1016/j.matbio.2024.02.009","DOIUrl":"10.1016/j.matbio.2024.02.009","url":null,"abstract":"<div><p>The largest mammalian organ, skin, consisting of a dermal connective tissue layer that underlies and supports the epidermis, acts as a protective barrier that excludes external pathogens and disseminates sensory signals emanating from the local microenvironment. Dermal connective tissue is comprised of a collagen-rich extracellular matrix (ECM) that is produced by connective tissue fibroblasts resident within the dermis. When wounded, a tissue repair program is induced whereby fibroblasts, in response to alterations in the microenvironment, produce new ECM components, resulting in the formation of a scar. Failure to terminate the normal tissue repair program causes fibrotic conditions including: hypertrophic scars, keloids, and the systemic autoimmune connective tissue disease scleroderma (systemic sclerosis, SSc). Histological and single-cell RNA sequencing (scRNAseq) studies have revealed that fibroblasts are heterogeneous and highly plastic. Understanding how this diversity contributes to dermal homeostasis, wounding, fibrosis, and cancer may ultimately result in novel anti-fibrotic therapies and personalized medicine. This review summarizes studies supporting this concept.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"128 ","pages":"Pages 31-38"},"PeriodicalIF":6.9,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X24000362/pdfft?md5=39f70e589c6770fd750b2ae39b89e2e3&pid=1-s2.0-S0945053X24000362-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139998107","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}

{"title":"Microvascular damage, neuroinflammation and extracellular matrix remodeling in Col18a1 knockout mice as a model for early cerebral small vessel disease","authors":"Mahsima Khoshneviszadeh ,&nbsp;Solveig Henneicke ,&nbsp;Daniel Pirici ,&nbsp;Akilashree Senthilnathan ,&nbsp;Lorena Morton ,&nbsp;Philipp Arndt ,&nbsp;Rahul Kaushik ,&nbsp;Oula Norman ,&nbsp;Jari Jukkola ,&nbsp;Ildiko Rita Dunay ,&nbsp;Constanze Seidenbecher ,&nbsp;Anne Heikkinen ,&nbsp;Stefanie Schreiber ,&nbsp;Alexander Dityatev","doi":"10.1016/j.matbio.2024.02.007","DOIUrl":"10.1016/j.matbio.2024.02.007","url":null,"abstract":"<div><p>Collagen type XVIII (COL18) is an abundant heparan sulfate proteoglycan in vascular basement membranes. Here, we asked (i) if the loss of COL18 would result in blood-brain barrier (BBB) breakdown, pathological alterations of small arteries and capillaries and neuroinflammation as found in cerebral small vessel disease (CSVD) and (ii) if such changes may be associated with remodeling of synapses and neural extracellular matrix (ECM). We found that 5-month-old <em>Col18a1^−/−</em> mice had elevated BBB permeability for mouse IgG in the deep gray matter, and intravascular erythrocyte accumulations were observed brain-wide in capillaries and arterioles. BBB permeability increased with age and affected cortical regions and the hippocampus in 12-month-old <em>Col18a1^−/−</em> mice. None of the <em>Col18a1^−/−</em> mice displayed hallmarks of advanced CSVD, such as hemorrhages, and did not show perivascular space enlargement. <em>Col18a1</em> deficiency-induced BBB leakage was accompanied by activation of microglia and astrocytes, a loss of aggrecan in the ECM of perineuronal nets associated with fast-spiking inhibitory interneurons and accumulation of the perisynaptic ECM proteoglycan brevican and the microglial complement protein C1q at excitatory synapses. As the pathway underlying these regulations, we found increased signaling through the TGF-ß1/Smad3/TIMP-3 cascade. We verified the pivotal role of COL18 for small vessel wall structure in CSVD by demonstrating the protein's involvement in vascular remodeling in autopsy brains from patients with cerebral hypertensive arteriopathy. Our study highlights an association between the alterations of perivascular ECM, extracellular proteolysis, and perineuronal/perisynaptic ECM, as a possible substrate of synaptic and cognitive alterations in CSVD.</p></div>","PeriodicalId":49851,"journal":{"name":"Matrix Biology","volume":"128 ","pages":"Pages 39-64"},"PeriodicalIF":6.9,"publicationDate":"2024-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0945053X2400026X/pdfft?md5=f5e54f1667086f5aee9e56f6e36957f1&pid=1-s2.0-S0945053X2400026X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139917019","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}