Cell Stress最新文献_第7页

Targeting FBXO44/SUV39H1 elicits tumor cell-specific DNA replication stress and viral mimicry. 靶向FBXO44/SUV39H1引发肿瘤细胞特异性DNA复制应激和病毒模仿。

IF 6.4

Cell Stress Pub Date : 2021-02-18 DOI: 10.15698/cst2021.03.245

Jia Z Shen, Charles Spruck

{"title":"Targeting FBXO44/SUV39H1 elicits tumor cell-specific DNA replication stress and viral mimicry.","authors":"Jia Z Shen, Charles Spruck","doi":"10.15698/cst2021.03.245","DOIUrl":"https://doi.org/10.15698/cst2021.03.245","url":null,"abstract":"Repetitive elements (REs) are normally transcriptionally silenced in somatic cells by repressive epigenetic modifications, which are thought to include DNA methylation and histone modifications such as deacetylation, H3K9me3, and H4K20me3. Although, it is unclear how RE silencing is maintained through DNA replication cycles in rapidly growing cancer cells. On the other hand, the reactivation of endogenous retroelements beyond a threshold level of tolerance in cancer cells, such as by treatment with DNA demethylating agents or HDAC or LSD1 inhibitors, can induce viral mimicry responses that augment certain cancer therapies, including immunotherapy. However, these agents can also affect normal cells presenting obvious side effects. Therefore, uncovering cancer cell-specific RE silencing mechanisms could provide a basis for the development of a new generation of cancer immunotherapy drugs. In our study (Shen et al. (2020), Cell, doi: 10.1016/j.cell.2020.11.042), through a high-content RNAi screen we identified FBXO44 as a key regulator of H3K9me3-mediated transcriptional silencing of REs in cancer cells. Inhibition of FBXO44 or its co-factor SUV39H1 stimulated antiviral pathways and interferon (IFN) signaling and induced replication stress and DNA double-strand breaks (DSBs) in cancer cells, leading to restricted tumor growth and synergy with anti-PD-1 therapy (Figure 1). Figure 1FIGURE 1: Graphical representation of this study.FBXO44/SUV39H1 targeting activates REs that elicit DNA replication stress and viral mimicry in cancer cells, leading to tumor growth arrest and enhanced immunotherapy response.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 3","pages":"37-39"},"PeriodicalIF":6.4,"publicationDate":"2021-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7921849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25446418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The OFD1 protein is a novel player in selective autophagy: another tile to the cilia/autophagy puzzle. OFD1蛋白是选择性自噬中的一个新角色:这是纤毛/自噬之谜的另一个拼图。

IF 6.4

Cell Stress Pub Date : 2021-02-17 DOI: 10.15698/cst2021.03.244

Manuela Morleo, Brunella Franco

{"title":"The OFD1 protein is a novel player in selective autophagy: another tile to the cilia/autophagy puzzle.","authors":"Manuela Morleo, Brunella Franco","doi":"10.15698/cst2021.03.244","DOIUrl":"https://doi.org/10.15698/cst2021.03.244","url":null,"abstract":"The autophagy-lysosomal pathway is one of the main degradative routes which cells use to balance sources of energy. A number of proteins orchestrate the formation of autophagosomes, membranous organelles instrumental in autophagy. Selective autophagy, involving the recognition and removal of specific targets, is mediated by autophagy receptors, which recognize cargos and the autophagosomal membrane protein LC3 for lysosomal degradation. Recently, bidirectional crosstalk has emerged between autophagy and primary cilia, microtubule-based sensory organelles extending from cells and anchored by the basal body, derived from the mother centriole of the centrosome. The molecular mechanisms underlying the direct role of autophagic proteins in cilia biology and, conversely, the impact of this organelle in autophagy remains elusive. Recently, we uncovered the molecular mechanism by which the centrosomal/basal body protein OFD1 controls the LC3-mediated autophagic cascade. In particular, we demonstrated that OFD1 acts as a selective autophagy receptor by regulating the turnover of unc-51-like kinase (ULK1) complex, which plays a crucial role in the initiation steps of autophagosome biogenesis. Moreover, we showed that patients with a genetic condition caused by mutations in OFD1 and associated with cilia dysfunction, display excessive autophagy and we demonstrated that autophagy inhibition significantly ameliorates the renal cystic phenotype in a conditional mouse model recapitulating the features of the disease (Morleo et al. 2020, EMBO J, doi: 10.15252/embj.2020105120). We speculate that abnormal autophagy may underlie some of the clinical manifestations observed in the disorders ascribed to cilia dysfunction.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 3","pages":"33-36"},"PeriodicalIF":6.4,"publicationDate":"2021-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7921851/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25446417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Innate RIG-I signaling restores antigen presentation in tumors and overcomes T cell resistance. 先天rig - 1信号恢复肿瘤中的抗原呈递并克服T细胞抵抗。

IF 6.4

Cell Stress Pub Date : 2021-01-18 DOI: 10.15698/cst2021.02.242

Beatrice Thier, Annette Paschen

{"title":"Innate RIG-I signaling restores antigen presentation in tumors and overcomes T cell resistance.","authors":"Beatrice Thier, Annette Paschen","doi":"10.15698/cst2021.02.242","DOIUrl":"https://doi.org/10.15698/cst2021.02.242","url":null,"abstract":"In recent years, therapy with immune modulating antibodies, termed immune checkpoint blockade (ICB), has revolutionized the treatment of advanced metastatic melanoma, yielding long-lasting clinical responses in a subgroup of patients. But despite this remarkable progress, resistance to therapy represents a major clinical challenge. ICB efficacy is critically dependent on cytotoxic CD8+ T cells targeting tumor cells in an HLA class I (HLA-I) antigen-dependent manner. Transcriptional suppression of the HLA-I antigen processing and presentation machinery (HLA-I APM) in melanoma cells leads to HLA-I-low/-negative tumor cell phenotypes escaping CD8+ T cell recognition and contributing to ICB resistance. In general, HLA-I-low/-negative tumor cells can be re-sensitized to T cells by interferons (IFN), augmenting HLA-I APM expression. However, this mechanism fails when melanoma cells acquire resistance to IFN, which recently turned out as a key resistance mechanism in ICB, besides HLA-I APM suppression. Seeking for a strategy to overcome these barriers, we identified a novel mechanism that restores HLA-I antigen presentation in tumor cells independent of IFN (Such et al. (2020) J Clin Invest, doi: 10.1172/JCI131572). We demonstrated that tumor cell-intrinsic activation of the cytosolic innate immunoreceptor RIG-I by its synthetic ligand 3pRNA overcomes transcriptional HLA-I APM suppression in patient-derived IFN-resistant melanoma cells. De novo HLA-I APM expression is IRF1/IRF3-dependent and re-sensitizes melanoma cells to autologous cytotoxic CD8+ T cells. Notably, synthetic RIG-I ligands and ICB synergize in T cell activation, suggesting combinational therapy could be an efficient strategy to improve patient outcomes in melanoma.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 2","pages":"26-28"},"PeriodicalIF":6.4,"publicationDate":"2021-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25342854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Improving glucose and lipids metabolism: drug development based on bile acid related targets. 改善葡萄糖和脂质代谢:基于胆汁酸相关靶点的药物开发。

IF 6.4

Cell Stress Pub Date : 2021-01-05 DOI: 10.15698/cst2021.01.239

Hanchen Shen, Lili Ding, Mehdi Baig, Jingyan Tian, Yang Wang, Wendong Huang

{"title":"Improving glucose and lipids metabolism: drug development based on bile acid related targets.","authors":"Hanchen Shen, Lili Ding, Mehdi Baig, Jingyan Tian, Yang Wang, Wendong Huang","doi":"10.15698/cst2021.01.239","DOIUrl":"https://doi.org/10.15698/cst2021.01.239","url":null,"abstract":"Bariatric surgery is one of the most effective treatment options for severe obesity and its comorbidities. However, it is a major surgery that poses several side effects and risks which impede its clinical use. Therefore, it is urgent to develop alternative safer pharmacological approaches to mimic bariatric surgery. Recent studies suggest that bile acids are key players in mediating the metabolic benefits of bariatric surgery. Bile acids can function as signaling molecules by targeting bile acid nuclear receptors and membrane receptors, like FXR and TGR5 respectively. In addition, the composition of bile acids is regulated by either the hepatic sterol enzymes such as CYP8B1 or the gut microbiome. These bile acid related targets all play important roles in regulating metabolism. Drug development based on these targets could provide new hope for patients without the risks of surgery and at a lower cost. In this review, we summarize the most updated progress on bile acid related targets and development of small molecules as drug candidates based on these targets.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 1","pages":"1-18"},"PeriodicalIF":6.4,"publicationDate":"2021-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784708/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38821304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Mitochondrial dynamics links PINCH-1 signaling to proline metabolic reprogramming and tumor growth. 线粒体动力学将PINCH-1信号与脯氨酸代谢重编程和肿瘤生长联系起来。

IF 6.4

Cell Stress Pub Date : 2020-12-10 DOI: 10.15698/cst2021.02.241

Ling Guo, Chuanyue Wu

{"title":"Mitochondrial dynamics links PINCH-1 signaling to proline metabolic reprogramming and tumor growth.","authors":"Ling Guo, Chuanyue Wu","doi":"10.15698/cst2021.02.241","DOIUrl":"https://doi.org/10.15698/cst2021.02.241","url":null,"abstract":"Proline metabolism is critical for cellular response to microenvironmental stress in living organisms across different kingdoms, ranging from bacteria, plants to animals. In bacteria and plants, proline is known to accrue in response to osmotic and other stresses. In higher organisms such as human, proline metabolism plays important roles in physiology as well as pathological processes including cancer. The importance of proline metabolism in physiology and diseases lies in the fact that the products of proline metabolism are intimately involved in essential cellular processes including protein synthesis, energy production and redox signaling. A surge of protein synthesis in fast proliferating cancer cells, for example, results in markedly increased demand for proline. Proline synthesis is frequently unable to meet the demand in fast proliferating cancer cells. The inadequacy of proline or \"proline vulnerability\" in cancer may provide an opportunity for therapeutic control of cancer progression. To this end, it is important to understand the signaling mechanism through which proline synthesis is regulated. In a recent study (Guo et al., Nat Commun 11(1):4913, doi: 10.1038/s41467-020-18753-6), we have identified PINCH-1, a component of cell-extracellular matrix (ECM) adhesions, as an important regulator of proline synthesis and cancer progression.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 2","pages":"23-25"},"PeriodicalIF":6.4,"publicationDate":"2020-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25342853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

To promote or inhibit glioma progression, that is the question for IL-33. 促进或抑制胶质瘤的进展，这是IL-33的问题。

IF 6.4

Cell Stress Pub Date : 2020-12-03 DOI: 10.15698/cst2021.01.240

Stephen M Robbins, Donna L Senger

{"title":"To promote or inhibit glioma progression, that is the question for IL-33.","authors":"Stephen M Robbins, Donna L Senger","doi":"10.15698/cst2021.01.240","DOIUrl":"https://doi.org/10.15698/cst2021.01.240","url":null,"abstract":"IL-33, a member of the IL-1 cytokine family has been shown to play a dual role within the body. First IL-33, similar to other IL-1 family members, is a secreted cytokine that binds to the cell surface receptor ST2 to induce a number of cell signaling pathways. Second, IL-33 enters the nucleus where it binds chromatin and directs transcriptional control of an array of growth factors and cytokines. Consistent with its complex cellular regulation, IL-33 mediates an array of biological functions by acting on a wide range of innate and adaptive immune cells. Recently, we found that IL-33 is expressed in a large number of human glioma patient specimens where its expression within the tumor correlates with the increased presence of Iba+ cells that include both resident microglia and recruited monocyte and macrophages. Strikingly, glioma derived expression of IL-33 correlates with a dramatic decrease in overall survival of tumor-bearing animals and thus supports its role as an influential factor in gliomagenesis. Notably however, when the nuclear localization function of IL-33 is crippled, the tumor microenvironment is programmed to be anti-tumorigenic and results in prolonged overall survival suggesting that when educated appropriately this could represent a novel therapeutic strategy for glioma (De Boeck et al. (2020), Nat Commun, doi: 10.1038/s41467-020-18569-4).","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"5 1","pages":"19-22"},"PeriodicalIF":6.4,"publicationDate":"2020-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38821303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AMPK maintains TCA cycle through sequential phosphorylation of PDHA to promote tumor metastasis. AMPK通过顺序磷酸化PDHA维持TCA循环，促进肿瘤转移。

IF 6.4

Cell Stress Pub Date : 2020-11-25 DOI: 10.15698/cst2020.12.238

Zhen Cai, Danni Peng, Hui-Kuan Lin

{"title":"AMPK maintains TCA cycle through sequential phosphorylation of PDHA to promote tumor metastasis.","authors":"Zhen Cai, Danni Peng, Hui-Kuan Lin","doi":"10.15698/cst2020.12.238","DOIUrl":"https://doi.org/10.15698/cst2020.12.238","url":null,"abstract":"Cancer represents the leading public health problem throughout the world. Globally, about one out of six deaths is related to cancer, which is largely due to the metastatic lesions. However, there are no effective strategies for targeting cancer metastasis. Identification of the key druggable targets maintaining metastasis is crucial for cancer treatment. In our recent study (Cai et al. (2020), Mol Cell, doi: 10.1016/j.molcel.2020.09.018), we found that activity of AMPK was enriched in metastatic tumors compared to primary tumors. Depletion of AMPK rendered cancer cells more sensitive to metabolic and oxidative stress, leading to the impairment of breast cancer lung metastasis. Activation of AMPK rewired cancer metabolism towards TCA cycle, which protects disseminated cancer cells from both metabolic and oxidative stress-induced cell death, and facilitates cancer metastasis. Further, AMPK critically maintained the activity of pyruvate dehydrogenase complex (PDH), the rate limiting enzyme involved in TCA cycle, thus favoring the pyruvate metabolism towards TCA cycle rather than converting it to lactate. Mechanistically, AMPK was shown to co-localize with PDHA, the catalytic subunit of PDH, in the mitochondrial matrix and directly triggered the phosphorylation of PDHA on Ser295 and Ser314. Hyper-phosphorylation of Ser295 and Ser314 of PDHA promotes lung metastasis through elevating activity of PDH. Of note, PDHA Ser314 phosphorylation abrogated the interaction between PDHA and PDHKs leading to the dephosphorylation on previously reported S293 site, whose phosphorylation serves as a negative signal for PDH activation, while S295 phosphorylation serves as an intrinsic catalytic site required for pyruvate metabolism. Our study presented the first evidence for the pro-metastatic property of the AMPK-PDH axis and advance our current understanding of how PDH is activated under physiological and pathological conditions.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"4 12","pages":"273-277"},"PeriodicalIF":6.4,"publicationDate":"2020-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38736467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

A sympathetic gut connection drives the metabolic benefits of Roux-en-Y gastric bypass. 交感肠连接驱动Roux-en-Y胃旁路术的代谢益处。

IF 6.4

Cell Stress Pub Date : 2020-11-24 DOI: 10.15698/cst2020.12.236

Mohammed K Hankir

引用次数: 2

TLR4: the fall guy in sepsis? TLR4:败血症的替罪羊?

IF 6.4

Cell Stress Pub Date : 2020-11-09 DOI: 10.15698/cst2020.12.237

Joseph Menassa, Christina Nedeva, Corey Pollock, Hamsa Puthalakath

{"title":"TLR4: the fall guy in sepsis?","authors":"Joseph Menassa, Christina Nedeva, Corey Pollock, Hamsa Puthalakath","doi":"10.15698/cst2020.12.237","DOIUrl":"https://doi.org/10.15698/cst2020.12.237","url":null,"abstract":"Sepsis and its impact on human health can be traced back to 1000 BC and continues to be a major health burden today. It causes about 11 million deaths world-wide of which, more than a third are due to neonatal sepsis. There is no effective treatment other than fluid resuscitation therapy and antibiotic treatment that leave patients immunosuppressed and vulnerable to nosocomial infections. Added to that, ageing population and the emergence of antibiotic resistant bacteria pose new challenges. Most of the deleterious effects of sepsis are due to the host response to the systemic infection. In the initial phase of infection, hyper activation of the immune system leads to cytokine storm, which could lead to organ failure and this accounts for about 15% of overall deaths. However, the subsequent immune paralysis phase (mostly attributed to apoptotic death of immune cells) accounts for about 85% of all deaths. Past clinical trials (more than 100 in the last 30 years) all targeted the inflammatory phase with little success, predictably, for inflammation is a necessary process to fight infection. In order to identify the regulators of immune cell death during sepsis, we carried out an unbiased, whole genome CRISPR screening in mice and identified Trigger Receptor Expressed in Myeloid-like 4 (Treml4) as the receptor that controls both the inflammatory phase and the immune suppression phase in sepsis (Nedeva et al. (2020) Nature Immunol, doi: 10.1038/s41590-020-0789-z). Characterising the Treml4 gene knockout mice revealed new insights into the relative roles of TLR4 and TREML4 in inducing the inflammatory cytokine storm during sepsis.","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"4 12","pages":"270-272"},"PeriodicalIF":6.4,"publicationDate":"2020-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7713263/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38736466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

A mutant p53/Hif1α/miR-30d axis reprograms the secretory pathway promoting the release of a prometastatic secretome. 突变的p53/Hif1α/miR-30d轴重编程分泌途径，促进原转移性分泌组的释放。

IF 6.4

Cell Stress Pub Date : 2020-10-05 DOI: 10.15698/cst2020.11.235

Valeria Capaci, Fiamma Mantovani, Giannino Del Sal

{"title":"A mutant p53/Hif1α/miR-30d axis reprograms the secretory pathway promoting the release of a prometastatic secretome.","authors":"Valeria Capaci, Fiamma Mantovani, Giannino Del Sal","doi":"10.15698/cst2020.11.235","DOIUrl":"https://doi.org/10.15698/cst2020.11.235","url":null,"abstract":"TP53 missense mutations are frequent driver events during tumorigenesis. The majority of TP53 mutations are missense and occur within the DNA binding domain of p53, leading to expression of mutant p53 (mut-p53) proteins that not only lose the tumor suppressive functions of the wild-type (wt-p53) form, but can also acquire novel oncogenic features fostering tumor growth, metastasis and chemoresistance. Mut-p53 affects fundamental cellular pathways and functions through different mechanisms, a major one being the alteration of gene expression. In our recent work (Capaci et al., 2020, Nat Commun) we found that mut-p53, via miR-30d, modifies structure and function of the Golgi apparatus (GA) and induces increased rate of trafficking. This culminates in the release of a pro-malignant secretome, which is capable of remodeling the tumor microenvironment (TME), to increase stiffness of the extracellular matrix (ECM), favouring metastatic colonization, as shown by cell-based assays and experiments of metastatic niche preconditioning in mouse xenograft models. This study provides new insights into the mechanisms by which mut-p53, through induction of non-coding RNAs, can exert pro-tumorigenic functions in a non-cell-autonomous fashion, and highlights potential non-invasive biomarkers and therapeutic targets to treat tumors harboring mut-p53 (Figure 1).","PeriodicalId":36371,"journal":{"name":"Cell Stress","volume":"4 11","pages":"261-264"},"PeriodicalIF":6.4,"publicationDate":"2020-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7590841/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38569855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1