Apoptosis最新文献

{"title":"Phosphatidylserine-mediated uptake of extracellular vesicles by hepatocytes ameliorates liver ischemia-reperfusion injury.","authors":"Rongrong Li, Chen Wang, Xiaoniao Chen, Enze Fu, Kaiyue Zhang, Hongyan Tao, Zhibo Han, Zhong-Chao Han, Zongjin Li","doi":"10.1007/s10495-024-02030-8","DOIUrl":"https://doi.org/10.1007/s10495-024-02030-8","url":null,"abstract":"<p><p>Compelling evidence suggests that mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) promote regeneration in animal models of liver injury by delivering signaling molecules. However, their target cells and uptake mechanism remain elusive. In this study, MSC-EVs were intravenously administered in a mouse model of liver ischemia-reperfusion injury (IRI). Our results revealed that MSC-EVs exhibit enhanced liver targeting in IRI mice, and injured hepatocytes display a greater capacity for MSC-EV uptake. We found that phosphatidylserine (PS) displayed on the exterior of injured hepatocytes promotes MSC-EV internalization, possibly by binding to MFGE8, a protein expressed on the MSC-EV membrane. Furthermore, the therapeutic effect of MSC-EVs on liver IRI is highly dependent on this PS-mediated uptake pathway. Our findings provide evidence that MSC-EVs preferentially target injured hepatocytes, relying on a PS-dependent uptake route to exert hepatoprotective effects, which are critical for the future design of EV-based therapeutic strategies for liver IRI.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IGF2BP3 boosts lactate generation to accelerate gastric cancer immune evasion","authors":"Kai Lin,&nbsp;Xiufeng Lin,&nbsp;Fan Luo","doi":"10.1007/s10495-024-02020-w","DOIUrl":"10.1007/s10495-024-02020-w","url":null,"abstract":"<div><p>The CD8⁺ T cells mediated antitumor immunity plays a critical function on gastric cancer (GC) immunotherapy. However, the mechanism of N⁶-methyladenosine (m⁶A) and lactate in GC immune microenvironment are still unclear. Here, present research investigated the role of Insulin like growth factor II mRNA binding protein 3 (IGF2BP3) in GC and its in-depth mechanisms in the antitumor immunity. Data illustrated that high IGF2BP3 level was associated to GC poor prognosis and tumor infiltration. Functional assays demonstrated that IGF2BP3 overexpression could promote the lactate accumulation, and impair the CD8⁺ T cells’ antitumor immunity activity in co-culture system. Correspondingly, IGF2BP3 silencing enhanced the CD8⁺ T cells’ antitumor immunity activity towards co-cultured GC cells. Mechanistically, IGF2BP3 could bind the m⁶A site on LDHA mRNA, thereby promoting its mRNA stability. Rescue assays elucidated that IGF2BP3/LDHA axis impaired the CD8⁺ T cells antitumor immunity by triggering lactate excess tumor microenvironment. In conclusion, our findings demonstrate that IGF2BP3 impairs the CD8⁺ T cells antitumor immunity by targeting LDHA/lactate axis, providing a novel therapeutic insight for GC immunotherapy.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel dual inhibitor targeting CDC25 and HDAC for treating triple-negative breast cancer","authors":"Bidyadhar Sethy,&nbsp;Richa Upadhyay,&nbsp;Iin Narwanti,&nbsp;Zih-Yao Yu,&nbsp;Sung-Bau Lee,&nbsp;Jing-Ping Liou","doi":"10.1007/s10495-024-02023-7","DOIUrl":"10.1007/s10495-024-02023-7","url":null,"abstract":"<div><p>Triple-negative breast cancer (TNBC) presents a significant challenge for treatment due to its aggressive nature and the lack of effective therapies. This study developed dual inhibitors against cell division cycle 25 (CDC25) and histone deacetylases (HDACs) for TNBC treatment. CDC25 phosphatases are crucial for activating cyclin-dependent kinases (CDKs), the master regulators of cell cycle progression. HDACs regulate various biological processes by deacetylating histone and non-histone proteins, affecting gene expression, chromatin structure, cell differentiation, and proliferation. Dysregulations of HDAC and CDC25 are associated with several human malignancies. We generated a group of dual inhibitors for CDC25 and HDAC by combining the molecular structures of CDC25 (quinoline-5,8-dione) and HDAC (hydroxamic acid or benzamide) pharmacophores. The newly developed compounds were evaluated against various solid-tumor, leukemia, and non-malignant breast epithelial cells. Among the synthesized compounds, <b>18A</b> emerged as a potent inhibitor, demonstrating significant cytotoxicity against TNBC cells, superior to its effects on other cancer types while sparing non-malignant cells. <b>18A</b> possessed similar HDAC inhibitory activity as MS-275 and potently suppressed CDC25 activity in vitro and the CDK1 dephosphorylation in cells. Additionally, <b>18A</b> hindered the progression of S and G₂/M phases, triggered DNA damage, and induced apoptosis. These findings underscore the potential of <b>18A</b> as a targeted therapy for TNBC and warrants further preclinical development.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><img></picture></div></div></figure></div></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142456624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sirtuin 7 ameliorates cuproptosis, myocardial remodeling and heart dysfunction in hypertension through the modulation of YAP/ATP7A signaling","authors":"Yu-Fei Chen,&nbsp;Rui-Qiang Qi,&nbsp;Jia-Wei Song,&nbsp;Si-Yuan Wang,&nbsp;Zhao-Jie Dong,&nbsp;Yi-Hang Chen,&nbsp;Ying Liu,&nbsp;Xin-Yu Zhou,&nbsp;Jing Li,&nbsp;Xiao-Yan Liu,&nbsp;Jiu-Chang Zhong","doi":"10.1007/s10495-024-02021-9","DOIUrl":"10.1007/s10495-024-02021-9","url":null,"abstract":"<div><p>Myocardial fibrosis is a typical pathological manifestation of hypertension. However, the exact role of sirtuin 7 (SIRT7) in myocardial remodeling remains largely unclear. Here, spontaneously hypertensive rats (SHRs) and angiotensin (Ang) II-induced hypertensive mice were pretreated with recombinant adeno-associated virus (rAAV)-SIRT7, copper chelator tetrathiomolybdate (TTM) or copper ionophore elesclomol, respectively. Compared with normotensive controls, reduced SIRT7 expression and augmented cuproptosis were observed in hearts of hypertensive rats and mice with decreased FDX1 levels and increased HSP70 levels. Notably, intervention with rAAV-SIRT7 and TTM strikingly prevented DLAT oligomers aggregation, and elevated ATP7A and TOM20 expressions, contributing to the alleviation of cuproptosis, mitochondrial injury, myocardial remodeling and heart dysfunction in spontaneously hypertensive rats and Ang II-induced hypertensive mice. In cultured rat primary cardiac fibroblasts (CFs), rhSIRT7 alleviated CuCl₂, Ang II or elesclomol-induced cuproptosis and fibroblast activation by blunting DLAT oligomers accumulation and downregulating α-SMA expression. Additionally, conditioned medium from rhSIRT7-pretreated CFs remarkably mitigated cellular hypertrophy and mitochondrial impairments of neonatal rat cardiomyocytes, as well as cell migration and polarization of RAW 264.7 macrophages. Importantly, verteporfin reduced CuCl₂-induced cuproptosis, mitochondrial injury and fibrotic activation in CFs. Knockdown of ATP7A with si-ATP7A blocked cellular protective effects of rhSIRT7 and verteporfin in CFs. In conclusion, SIRT7 attenuates cuproptosis, myocardial fibrosis and heart dysfunction in hypertension through the modulation of YAP/ATP7A signaling. Targeting SIRT7 is of vital importance for developing therapeutic strategies in hypertension and hypertensive heart disorders.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142405949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated serum mtDNA in COVID-19 patients is linked to SARS-CoV-2 envelope protein targeting mitochondrial VDAC1, inducing apoptosis and mtDNA release","authors":"Anna Shteinfer-Kuzmine,&nbsp;Ankit Verma,&nbsp;Rut Bornshten,&nbsp;Eli Ben Chetrit,&nbsp;Ami Ben-Ya’acov,&nbsp;Hadas Pahima,&nbsp;Ethan Rubin,&nbsp;Yosef Mograbi,&nbsp;Eyal Shteyer,&nbsp;Varda Shoshan-Barmatz","doi":"10.1007/s10495-024-02025-5","DOIUrl":"10.1007/s10495-024-02025-5","url":null,"abstract":"<div><p>Mitochondria dysfunction is implicated in cell death, inflammation, and autoimmunity. During viral infections, some viruses employ different strategies to disrupt mitochondria-dependent apoptosis, while others, including SARS-CoV-2, induce host cell apoptosis to facilitate replication and immune system modulation. Given mitochondrial DNAs (mtDNA) role as a pro-inflammatory damage-associated molecular pattern in inflammatory diseases, we examined its levels in the serum of COVID-19 patients and found it to be high relative to levels in healthy donors. Furthermore, comparison of serum protein profiles between healthy individuals and SARS-CoV-2-infected patients revealed unique bands in the COVID-19 patients. Using mass spectroscopy, we identified over 15 proteins, whose levels in the serum of COVID-19 patients were 4- to 780-fold higher. As mtDNA release from the mitochondria is mediated by the oligomeric form of the mitochondrial-gatekeeper—the voltage-dependent anion-selective channel 1 (VDAC1)—we investigated whether SARS-CoV-2 protein alters VDAC1 expression. Among the three selected SARS-CoV-2 proteins, small envelope (E), nucleocapsid (N), and accessory 3b proteins, the E-protein induced VDAC1 overexpression, VDAC1 oligomerization, cell death, and mtDNA release. Additionally, this protein led to mitochondrial dysfunction, as evidenced by increased mitochondrial ROS production and cytosolic Ca²⁺ levels. These findings suggest that SARS-CoV-2 E-protein induces mitochondrial dysfunction, apoptosis, and mtDNA release via VDAC1 modulation. mtDNA that accumulates in the blood activates the cGAS-STING pathway, triggering inflammatory cytokine and chemokine expression that contribute to the cytokine storm and tissue damage seen in cases of severe COVID-19.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11550248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging druggable targets for immune checkpoint modulation in cancer immunotherapy: the iceberg lies beneath the surface","authors":"Sakuntala Gayen,&nbsp;Swarupananda Mukherjee,&nbsp;Sandipan Dasgupta,&nbsp;Souvik Roy","doi":"10.1007/s10495-024-02022-8","DOIUrl":"10.1007/s10495-024-02022-8","url":null,"abstract":"<div><p>The immune system serves as a fundamental defender against the initiation and progression of cancer. Failure of the immune system augments immunosuppressive action that leading to cancer manifestation. This immunosuppressive effect causes from significant alterations in immune checkpoint expression associated with tumoral progression. The tumor microenvironment promotes immune escape mechanisms that further amplifying immunosuppressive actions. Notably, substantial targeting of immune checkpoints has been pragmatic in the advancement of cancer research. This study highlights a comprehensive review of emerging druggable targets aimed at modulating immune checkpoint co-inhibitory as well as co-stimulatory molecules in response to immune system activation. This modulation has prompted to the development of newer therapeutic insights, eventually inducing immunogenic cell death through immunomodulatory actions. The study emphasizes the role of immune checkpoints in immunogenic regulation of cancer pathogenesis and explores potential therapeutic avenues in cancer immunotherapy.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div><p>Modulation of Immunosuppressive and Immunostimulatory pathways of immune checkpoints in cancer immunotherapy</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-PD-L1 blockade facilitates antitumor effects of radiofrequency ablation by improving tumor immune microenvironment in hepatocellular carcinoma.","authors":"Jiahua Liang, Mingjian Ma, Wei Feng, Qiongcong Xu, Dong Chen, Jiaming Lai, Jiancong Chen","doi":"10.1007/s10495-024-02019-3","DOIUrl":"https://doi.org/10.1007/s10495-024-02019-3","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a complex disease with advanced presentation that significantly affects survival rates. Therefore, novel therapeutic strategies are needed. In this study, we investigate the tumor microenvironment (TME) in HCC by analyzing 13 HCC samples at single cell level. We identified key cell populations, including CD8 + T cells, Tregs, M1/M2 macrophages, and CD4 + memory T cells, and explored their roles and interactions. Our research revealed an early enrichment of CD8 + T cells, which could potentially lead to their exhaustion and facilitate tumor progression. We also investigated the impact of percutaneous radiofrequency ablation (RFA) on the immune microenvironment. Using a dual tumor mouse model, we demonstrated that RFA induces necrosis, enhancing antigen presentation and altering immune responses. Our results indicate that RFA increases PD-L1 expression in residual liver tissue, suggesting potential immune escape mechanisms. Furthermore, the combination of RFA and anti-PD-L1 therapy in the mouse model resulted in significant improvements in immune modulation. This included increased CD8 + T cell efficacy and decreased Treg infiltration. This combination shows promise as an approach to counteract HCC progression by altering the immune landscape. This study highlights the critical interaction within the TME of HCC and suggests the possibility of improving patient outcomes by targeting immune evasion mechanisms through combined therapeutic strategies.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"β-glucan nanoparticles alleviate acute asthma by suppressing ferroptosis and DNA damage in mice.","authors":"Bassam W Ebeed, Islam Ahmed Abdelmawgood, Mohamed A Kotb, Noha A Mahana, Ayman Saber Mohamed, Marwa A Ramadan, Abeer Mahmoud Badr, Manar Nasr, Osama Mohsen Qurani, Reem Mohamed Hamdy, Nada Yasser Abd El-Hakiem, Mariam Khaled Fahim, Mariam Morris Fekry, Jehane I Eid","doi":"10.1007/s10495-024-02013-9","DOIUrl":"https://doi.org/10.1007/s10495-024-02013-9","url":null,"abstract":"<p><p>Asthma is a severe respiratory disease marked by airway inflammation, remodeling, and oxidative stress. β-Glucan (BG), a polysaccharide constituent of fungal cellular structures, exhibits potent immunomodulatory activities. The investigational focus was on the anti-asthmatic and anti-ferroptotic properties of beta-glucan nanoparticles (BG-NPs) in a murine model of allergic asthma induced by ovalbumin (OVA). BG was extracted from Chaga mushrooms (Inonotus obliquus), and its BG-NPs were characterized utilizing techniques including FT-IR, UV visible spectroscopy, zeta potential analysis, DLS, XRD, and TEM. The Balb/C mice were allocated into five groups: control, untreated asthmatic, dexamethasone (Dexa)-treated (1 mg/kg), BG-treated (100 mg/kg), BG-NPs-treated (45 mg/kg), and BG-treated (100 mg/kg). Treatment with BG-NPs markedly diminished the entry of inflammatory cells into the respiratory passage, serum IgE concentrations, DNA damage, and markers of oxidative stress through the reduction of malonaldehyde (MDA) levels and enhancing the levels of reduced glutathione (GSH), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). Furthermore, BG-NPs reduced iron deposition and promoted the transcriptional activity of the GPx4 gene in pulmonary cells, attenuating ferroptosis. The results demonstrated that BG-NPs reduced asthma by inhibiting oxidative stress, inflammation, DNA damage, and ferroptosis. Our results suggest that BG-NPs could be used as potential treatments for allergic asthma.</p>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GPR37 promotes colorectal cancer against ferroptosis by reprogramming lipid metabolism via p38-SCD1 axis","authors":"Jiamin Zhou,&nbsp;Xigan He,&nbsp;Weixing Dai,&nbsp;Qingguo Li,&nbsp;Zhen Xiang,&nbsp;Yixiu Wang,&nbsp;Ti Zhang,&nbsp;Weiqi Xu,&nbsp;Lu Wang,&nbsp;Anrong Mao","doi":"10.1007/s10495-024-02018-4","DOIUrl":"10.1007/s10495-024-02018-4","url":null,"abstract":"<div><p>Colorectal cancer (CRC) is a prevalent malignant tumor worldwide, leading to significant morbidity and disease burden. Diagnostic indicators and treatment objectives for CRC are urgently needed. This study demonstrates that GPR37, a GPCR receptor, is highly expressed in CRC. Depletion of GPR37 significantly reduced CRC tumor cell growth both in vitro and in vivo. Further tests showed that GPR37 protects cancer cells from ferroptosis by upregulating SCD1 expression, thereby modulating lipid metabolism, suppressing the level of reactive oxygen species, and mitigating ferroptosis. Mechanistic studies have shown that GPR37 modulates lipid metabolism in tumor cells by promoting SCD1 transcription via the MAPK-p38 signaling pathway. Our results reveal the pro-carcinogenic effect of GPR37 in primary CRC and suggest that targeting GPR37 could be a potential therapeutic target for CRC.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is long-term administration of PLD-pegylated liposomal doxorubicin able to induce oral cancer?","authors":"Arjun Pandian,&nbsp;Azhagu Madhavan Sivalingam","doi":"10.1007/s10495-024-02017-5","DOIUrl":"10.1007/s10495-024-02017-5","url":null,"abstract":"<div><p>Leukoplakia, a potentially malignant oral condition, manifests as a nonremovable white lesion that is often linked to risk factors such as smoking, alcohol, and HPV. Pegylated liposomal doxorubicin (PLD), which is used in cancer treatment, has been associated with secondary oral cancers, particularly in patients with leukoplakia. A case study revealed the development of squamous cell carcinoma (SCC) on the tongue following PLD treatment, suggesting a potential link between the drug and malignant transformation. Despite the benefits of PLD in reducing cardiac toxicity, long-term oral monitoring is essential due to the persistent risk of oral cancer posttreatment.</p></div>","PeriodicalId":8062,"journal":{"name":"Apoptosis","volume":null,"pages":null},"PeriodicalIF":6.1,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142144994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}