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  1. Article: Metagenomic next-generation sequencing for pleural effusions induced by viral pleurisy: A case report.

    Liu, Xue-Ping / Mao, Chen-Xue / Wang, Guan-Song / Zhang, Ming-Zhou

    World journal of clinical cases

    2023  Volume 11, Issue 4, Page(s) 844–851

    Abstract: Background: Viral pleurisy is a viral infected disease with exudative pleural effusions. It is one of the causes for pleural effusions. Because of the difficult etiology diagnosis, clinically pleural effusions tend to be misdiagnosed as tuberculous ... ...

    Abstract Background: Viral pleurisy is a viral infected disease with exudative pleural effusions. It is one of the causes for pleural effusions. Because of the difficult etiology diagnosis, clinically pleural effusions tend to be misdiagnosed as tuberculous pleurisy or idiopathic pleural effusion. Here, we report a case of pleural effusion secondary to viral pleurisy which is driven by infection with epstein-barr virus. Viral infection was identified by metagenomic next-generation sequencing (mNGS).
    Case summary: A 40-year-old male with a history of dermatomyositis, rheumatoid arthritis, and secondary interstitial pneumonia was administered with long-term oral prednisone. He presented with fever and chest pain after exposure to cold, accompanied by generalized sore and weakness, night sweat, occasional cough, and few sputums. The computed tomography scan showed bilateral pleural effusions and atelectasis of the partial right lower lobe was revealed. The pleural fluids were found to be yellow and slightly turbid after pleural catheterization. Thoracoscopy showed fibrous adhesion and auto-pleurodesis. Combining the results in pleural fluid analysis and mNGS, the patient was diagnosed as viral pleuritis. After receiving Aciclovir, the symptoms and signs of the patient were relieved.
    Conclusion: Viral infection should be considered in cases of idiopathic pleural effusion unexplained by routine examination. mNGS is helpful for diagnosis.
    Language English
    Publishing date 2023-01-06
    Publishing country United States
    Document type Case Reports
    ISSN 2307-8960
    ISSN 2307-8960
    DOI 10.12998/wjcc.v11.i4.844
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Role of plasma TNF-α and IL-6 levels in prediction of acute respiratory distress syndrome based on their synchronous detection

    GAN Zhixin / HE Binfeng / XU Jiancheng / WANG Guansong / XU Zhi

    Di-san junyi daxue xuebao, Vol 42, Iss 5, Pp 493-

    2020  Volume 498

    Abstract: Objective To investigate the role of plasma TNF-α and IL-6 levels in prediction of occurrence of acute respiratory distress syndrome (ARDS) in high-risk patients. Methods A total of 30 patients who were at high risk for ARDS and enrolled in ICU of our ... ...

    Abstract Objective To investigate the role of plasma TNF-α and IL-6 levels in prediction of occurrence of acute respiratory distress syndrome (ARDS) in high-risk patients. Methods A total of 30 patients who were at high risk for ARDS and enrolled in ICU of our Center of Respiratory and Critical Care Medicine from June 2018 to April 2019 were subjected in this study. Among them, 13 developed into ARDS (ARDS group), and the other 17 served as high risk group. Their clinical data and plasma samples at admission were collected. Plasma samples from 18 heath volunteers were also harvested. The soluble proteins, TNF-α and IL-6, in the samples were quantitatively detected by flow cytometry. Results The plasma levels of TNF-α and IL-6 were significantly higher in the ARDS patients than the high risk group and health control, while those in the high risk group also higher than those in the health control group (P < 0.05). The TNF-α level was closely associated with the progression of ARDS in high-risk patients. Furthermore, the patients of the ARDS group had significantly higher APACHE-Ⅱ score and higher levels of C-reactive protein, procalcitonin, direct bilirubin and lactic acid, while obviously lower oxygenation index and albumin level when compared with the high risk group (P < 0.05). Finally, from the 30 high risk patients, 15 died and 15 survived, and there were no notable differences in the TNF-α and IL-6 levels between the dead and survival (P>0.05). But the dead still had remarkably higher APACHE-Ⅱ score and levels of C-reactive protein, urea and uric acid, while obviously lower albumin, total plasma protein and oxygenation index than the survival (P < 0.05). Conclusion The plasma TNF-α level at admission is closely associated with the progression of ARDS in high-risk patients, and might be regarded as a marker to predict its occurrence.
    Keywords acute respiratory distress syndrome ; tnf-α ; il-6 ; inflammation ; Medicine (General) ; R5-920
    Subject code 610
    Language Chinese
    Publishing date 2020-03-01T00:00:00Z
    Publisher Editorial Office of Journal of Third Military Medical University
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: The TLR7/8 agonist R848 optimizes host and tumor immunity to improve therapeutic efficacy in murine lung cancer.

    Zhou, Jianchun / Xu, Yu / Wang, Guansong / Mei, Tonghua / Yang, Hao / Liu, Yuliang

    International journal of oncology

    2022  Volume 61, Issue 1

    Abstract: Treatment with the Toll‑like receptor 7 (TLR7) agonist, resiquimod (R848), is effective in various types of cancer, such as breast, pancreatic and colorectal cancer. The reported antitumor effect of R848 in lung cancer is considered to be achieved by ... ...

    Abstract Treatment with the Toll‑like receptor 7 (TLR7) agonist, resiquimod (R848), is effective in various types of cancer, such as breast, pancreatic and colorectal cancer. The reported antitumor effect of R848 in lung cancer is considered to be achieved by targeting macrophages. In the present study, it was demonstrated that TLR7 expression on various immune cell types initially rises, then declines in the late stage of lung cancer. Intraperitoneal injection of R848 resulted in a reduction in tumor burden and prolonged survival in both subcutaneous and metastatic lung cancer models in C57BL/6 mice. Initial treatment with R848 at an early stage was found to be the optimal choice. Systemic injection of R848 promoted the activation of innate and adaptive immune responses. Systemic administration of R848 upregulated TLR7 expression in dendritic cells (DCs) and enhanced the activation of DCs and natural killer (NK) cells. Moreover, this treatment also resulted in increased production of T helper cell‑associated cytokines in serum, including IFN‑γ, TNF‑α and IL‑2. In addition, continuous treatment with R848 increased the proportion of DCs, NK and CD8
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/metabolism ; Humans ; Immunotherapy/methods ; Lung Neoplasms/drug therapy ; Mice ; Mice, Inbred C57BL ; Toll-Like Receptor 7 ; Tumor Microenvironment
    Chemical Substances TLR7 protein, human ; Toll-Like Receptor 7
    Language English
    Publishing date 2022-05-13
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 1154403-x
    ISSN 1791-2423 ; 1019-6439
    ISSN (online) 1791-2423
    ISSN 1019-6439
    DOI 10.3892/ijo.2022.5371
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Rab26 promotes macrophage phagocytosis through regulation of MFN2 trafficking to mitochondria.

    Wu, Di / Wang, Yao / Hu, Junxian / Xu, Yuhang / Gong, Daohui / Wu, Pengfei / Dong, Junkang / He, Binfeng / Qian, Hang / Wang, Guansong

    The FEBS journal

    2023  Volume 290, Issue 16, Page(s) 4023–4039

    Abstract: Acute respiratory distress syndrome (ARDS) is an inflammatory disorder of the lungs caused by bacterial or viral infection. Timely phagocytosis and clearance of pathogens by macrophages are important in controlling inflammation and alleviating ARDS. ... ...

    Abstract Acute respiratory distress syndrome (ARDS) is an inflammatory disorder of the lungs caused by bacterial or viral infection. Timely phagocytosis and clearance of pathogens by macrophages are important in controlling inflammation and alleviating ARDS. However, the precise mechanism of macrophage phagocytosis remains to be explored. Here, we show that the expression of Rab26 is increased in Escherichia coli- or Pseudomonas aeruginosa-stimulated bone marrow-derived macrophages. Knocking out Rab26 reduced phagocytosis and bacterial clearance by macrophages. Rab26 interacts with mitochondrial fusion protein mitofusin-2 (MFN2) and affects mitochondrial reactive oxygen species generation by regulating MFN2 transport. The levels of MFN2 in mitochondria were reduced in Rab26-deficient bone marrow-derived macrophages, and the levels of mitochondrial reactive oxygen species and ATP were significantly decreased. Knocking down MFN2 using small interfering RNA resulted in decreased phagocytosis and killing ability of macrophages. Rab26 knockout reduced phagocytosis and bacterial clearance by macrophages in vivo, significantly increased inflammatory factors, aggravated lung tissue damage, and increased mortality in mice. Our results demonstrate that Rab26 regulates phagocytosis and clearance of bacteria by mediating the transport of MFN2 to mitochondria in macrophages, thus alleviating ARDS in mice and potentially in humans.
    MeSH term(s) Humans ; Mice ; Animals ; Reactive Oxygen Species/metabolism ; Phagocytosis/genetics ; Macrophages/metabolism ; Hydrolases/metabolism ; Bacteria/metabolism ; Respiratory Distress Syndrome/metabolism ; Mitochondria/metabolism ; GTP Phosphohydrolases/genetics ; GTP Phosphohydrolases/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
    Chemical Substances Reactive Oxygen Species ; Hydrolases (EC 3.-) ; MFN2 protein, human (EC 3.6.1.-) ; GTP Phosphohydrolases (EC 3.6.1.-) ; Mitochondrial Proteins ; Rab26 protein, human (EC 3.6.1.-.) ; rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2023-05-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16793
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Rab26 alleviates sepsis-induced immunosuppression as a master regulator of macrophage ferroptosis and polarization shift.

    Gong, Daohui / Liu, Xueping / Wu, Pengfei / Chen, Yue / Xu, Yuhang / Gao, Zhan / Qian, Hang / Wang, Guansong / He, Binfeng

    Free radical biology & medicine

    2023  Volume 212, Page(s) 271–283

    Abstract: Macrophage dysfunction is a significant contributor to more than 70 % of sepsis-related deaths, specifically secondary bacterial infections, during the immunosuppression stage of sepsis. Nevertheless, the role of Rab26 in this context remains unclear. In ...

    Abstract Macrophage dysfunction is a significant contributor to more than 70 % of sepsis-related deaths, specifically secondary bacterial infections, during the immunosuppression stage of sepsis. Nevertheless, the role of Rab26 in this context remains unclear. In this study, we observed a substantial decrease in Rab26 expression in macrophages during the immunosuppressive phase of sepsis, which was also found to be suppressed by high extracellular levels of HMGB1. During the progression of sepsis, Rab26 deficiency promotes a polarization shift from the M1 to the M2-like phenotype in macrophages, rendering them susceptible to ferroptosis. Subsequent experimentation has revealed that Rab26 deficiency facilitates the degradation of GPX4, thereby aggravating macrophage ferroptosis through the upregulation of levels of lipid ROS, MDA, and ferrous iron induced by RSL3, a ferroptosis inducer. Additionally, Rab26-deficient mice in the immunosuppressed phase of sepsis exhibit heightened susceptibility to secondary infections, leading to exacerbated lung tissue damage and increased mortality rate. Overall, these findings indicate that Rab26 plays a crucial role in sepsis-induced macrophage immunosuppression by regulating macrophage ferroptosis and polarization. Hence, it represents a potential novel target for sepsis therapy.
    MeSH term(s) Animals ; Mice ; Ferroptosis/genetics ; Immunosuppression Therapy ; Sepsis/genetics ; Immunosuppressive Agents ; Macrophages
    Chemical Substances Immunosuppressive Agents
    Language English
    Publishing date 2023-12-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2023.12.046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Sunflower pollen-derived microcapsules adsorb light and bacteria for enhanced antimicrobial photothermal therapy.

    Yang, Yao / Wang, Bin / Liu, Qian / Wei, Zhenghua / Mou, Ziye / Li, Quan / Chen, Chunfa / You, Zaichun / Li, Bang Lin / Wang, Guansong / Xu, Zhi / Qian, Hang

    Nanoscale

    2024  

    Abstract: Bacterial infection is one of the most serious clinical complications, with life-threatening outcomes. Nature-inspired biomaterials offer appealing microscale and nanoscale architectures that are often hard to fabricate by traditional technologies. ... ...

    Abstract Bacterial infection is one of the most serious clinical complications, with life-threatening outcomes. Nature-inspired biomaterials offer appealing microscale and nanoscale architectures that are often hard to fabricate by traditional technologies. Inspired by the light-harvesting nature, we engineered sulfuric acid-treated sunflower sporopollenin exine-derived microcapsules (HSECs) to capture light and bacteria for antimicrobial photothermal therapy. Sulfuric acid-treated HSECs show a greatly enhanced photothermal performance and a strong bacteria-capturing ability against Gram-positive bacteria. This is attributed to the hierarchical micro/nanostructure and surface chemistry alteration of HSECs. To test the potential for clinical application, an
    Language English
    Publishing date 2024-04-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2515664-0
    ISSN 2040-3372 ; 2040-3364
    ISSN (online) 2040-3372
    ISSN 2040-3364
    DOI 10.1039/d3nr04814d
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Tobramycin-mediated self-assembly of DNA nanostructures for targeted treatment of

    Xu, Yuhang / Liu, Qian / Wang, Bin / Li, Quan / Chen, Yue / Yang, Yao / Zhu, Zhihao / Gong, Daohui / Zhang, Chuan / Wang, Guansong / Qian, Hang

    Biomaterials science

    2024  Volume 12, Issue 9, Page(s) 2331–2340

    Abstract: Pseudomonas ... ...

    Abstract Pseudomonas aeruginosa
    MeSH term(s) Pseudomonas aeruginosa/drug effects ; Tobramycin/pharmacology ; Tobramycin/administration & dosage ; Tobramycin/chemistry ; Animals ; Pseudomonas Infections/drug therapy ; Pseudomonas Infections/microbiology ; Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/chemistry ; Anti-Bacterial Agents/administration & dosage ; Nanostructures/chemistry ; Nanostructures/administration & dosage ; Mice ; DNA/chemistry ; DNA/administration & dosage ; Pneumonia/drug therapy ; Pneumonia/microbiology ; Humans ; Biofilms/drug effects ; Microbial Sensitivity Tests
    Chemical Substances Tobramycin (VZ8RRZ51VK) ; Anti-Bacterial Agents ; DNA (9007-49-2)
    Language English
    Publishing date 2024-04-30
    Publishing country England
    Document type Journal Article
    ZDB-ID 2693928-9
    ISSN 2047-4849 ; 2047-4830
    ISSN (online) 2047-4849
    ISSN 2047-4830
    DOI 10.1039/d3bm02121a
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Rab26 promotes macrophage phagocytosis through regulation of MFN2 trafficking to mitochondria

    Wu, Di / Wang, Yao / Hu, Junxian / Xu, Yuhang / Gong, Daohui / Wu, Pengfei / Dong, Junkang / He, Binfeng / Qian, Hang / Wang, Guansong

    The FEBS Journal. 2023 Aug., v. 290, no. 16 p.4023-4039

    2023  

    Abstract: Acute respiratory distress syndrome (ARDS) is an inflammatory disorder of the lungs caused by bacterial or viral infection. Timely phagocytosis and clearance of pathogens by macrophages are important in controlling inflammation and alleviating ARDS. ... ...

    Abstract Acute respiratory distress syndrome (ARDS) is an inflammatory disorder of the lungs caused by bacterial or viral infection. Timely phagocytosis and clearance of pathogens by macrophages are important in controlling inflammation and alleviating ARDS. However, the precise mechanism of macrophage phagocytosis remains to be explored. Here, we show that the expression of Rab26 is increased in Escherichia coli‐ or Pseudomonas aeruginosa‐stimulated bone marrow‐derived macrophages. Knocking out Rab26 reduced phagocytosis and bacterial clearance by macrophages. Rab26 interacts with mitochondrial fusion protein mitofusin‐2 (MFN2) and affects mitochondrial reactive oxygen species generation by regulating MFN2 transport. The levels of MFN2 in mitochondria were reduced in Rab26‐deficient bone marrow‐derived macrophages, and the levels of mitochondrial reactive oxygen species and ATP were significantly decreased. Knocking down MFN2 using small interfering RNA resulted in decreased phagocytosis and killing ability of macrophages. Rab26 knockout reduced phagocytosis and bacterial clearance by macrophages in vivo, significantly increased inflammatory factors, aggravated lung tissue damage, and increased mortality in mice. Our results demonstrate that Rab26 regulates phagocytosis and clearance of bacteria by mediating the transport of MFN2 to mitochondria in macrophages, thus alleviating ARDS in mice and potentially in humans.
    Keywords Escherichia ; Pseudomonas ; RNA ; acute respiratory distress syndrome ; inflammation ; lungs ; macrophages ; mitochondria ; mortality ; phagocytosis ; reactive oxygen species
    Language English
    Dates of publication 2023-08
    Size p. 4023-4039.
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note JOURNAL ARTICLE
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.16793
    Database NAL-Catalogue (AGRICOLA)

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  9. Article ; Online: Extracellular HMGB1 Impairs Macrophage-Mediated Efferocytosis by Suppressing the Rab43-Controlled Cell Surface Transport of CD91.

    Wang, Yao / Zhang, Wen / Xu, Yu / Wu, Di / Gao, Zhan / Zhou, Jianchun / Qian, Hang / He, Binfeng / Wang, Guansong

    Frontiers in immunology

    2022  Volume 13, Page(s) 767630

    Abstract: High-mobility group box 1 (HMGB1) protein can impair phagocyte function by suppressing the macrophage-mediated clearance of apoptotic cells (ACs), thereby delaying inflammation resolution in the lungs and allowing the progression of acute lung injury ( ... ...

    Abstract High-mobility group box 1 (HMGB1) protein can impair phagocyte function by suppressing the macrophage-mediated clearance of apoptotic cells (ACs), thereby delaying inflammation resolution in the lungs and allowing the progression of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). However, the precise mechanism underlying this HMGB1-mediated inhibition of efferocytosis remains unknown. The aim of this study was to determine the effect of HMGB1 on macrophage-mediated efferocytosis. We discovered that HMGB1 prevented efferocytosis by bone marrow-derived macrophages (BMDMs) and suppressed the expression of Ras-related GTP-binding protein 43 (Rab43), a member of the Ras-associated binding (Rab) family. The downregulation of Rab43 expression resulted in impaired clearance of apoptotic thymocytes by BMDMs. Subsequent analysis of HMGB1-treated and Rab43-deficient BMDMs revealed the inhibited transport of cluster of differentiation 91 (CD91), a phagocyte recognition receptor, from the cytoplasm to the cell surface. Notably, Rab43 directly interacted with CD91 to mediate its intercellular trafficking. Furthermore, Rab43 knockout delayed the inflammation resolution and aggravated the lung tissue damage in mice with ALI. Therefore, our results provide evidence that HMGB1 impairs macrophage-mediated efferocytosis and delays inflammation resolution by suppressing the Rab43-regulated anterograde transport of CD91, suggesting that the restoration of Rab43 levels is a promising strategy for attenuating ALI and ARDS in humans.
    MeSH term(s) Acute Lung Injury/metabolism ; Animals ; HMGB1 Protein/metabolism ; Inflammation/metabolism ; Low Density Lipoprotein Receptor-Related Protein-1/metabolism ; Macrophages/metabolism ; Mice ; Phagocytosis ; Respiratory Distress Syndrome ; rab GTP-Binding Proteins/metabolism
    Chemical Substances HMGB1 Protein ; HMGB1 protein, mouse ; Low Density Lipoprotein Receptor-Related Protein-1 ; Lrp1 protein, mouse ; Rab44 protein, mouse (EC 3.6.5.2) ; rab GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2022-03-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.767630
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Framework Nucleic Acids Enabled Pulmonary Artery Endothelial Cell Growth Inhibition by Targeting microRNA-152.

    You, Zaichun / Huang, Qiuhong / Xu, Lilin / Liu, Xueping / Fu, Juan / Li, Boxuan / Yang, Yi / Li, Shuyi / Qian, Hang / Wang, Guansong

    Chembiochem : a European journal of chemical biology

    2022  Volume 23, Issue 18, Page(s) e202200344

    Abstract: Pulmonary artery vascular endothelial dysfunction plays a pivotal role in the occurrence and progression of pulmonary vascular remodeling (PVR). To address this, aberrantly expressed non-coding microRNAs (miRNAs) are excellent therapeutic targets in ... ...

    Abstract Pulmonary artery vascular endothelial dysfunction plays a pivotal role in the occurrence and progression of pulmonary vascular remodeling (PVR). To address this, aberrantly expressed non-coding microRNAs (miRNAs) are excellent therapeutic targets in human pulmonary artery endothelial cells (HPAECs). Here, we discovered and validated the overexpression of miRNA-152 in HPAECs under hypoxia and its role in endothelial cell dysfunction. We constructed a framework nucleic acid nanostructure that harbors six protruding single-stranded DNA segments that can fully hybridize with miRNA-152 (DNT-152). DNT-152 was efficiently taken up by HPAECs with increasing time and concentration; it markedly induced apoptosis, and inhibited HPAEC growth under hypoxic conditions. Mechanistically, DNT-152 silenced miRNA-152 expression and upregulated its target gene Meox2, which subsequently inhibited the AKT/mTOR signaling pathway. These results indicate that miRNA-152 in HPAECs may be an excellent therapeutic target against PVR, and that framework nucleic acids with carefully designed sequences are promising nanomedicines for noncancerous cells and diseases.
    MeSH term(s) Humans ; Cell Proliferation ; DNA, Single-Stranded/metabolism ; Endothelial Cells/metabolism ; Hypoxia/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Nucleic Acids/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Pulmonary Artery/metabolism ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances DNA, Single-Stranded ; MicroRNAs ; MIRN152 microRNA, human ; Nucleic Acids ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2022-08-11
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020469-3
    ISSN 1439-7633 ; 1439-4227
    ISSN (online) 1439-7633
    ISSN 1439-4227
    DOI 10.1002/cbic.202200344
    Database MEDical Literature Analysis and Retrieval System OnLINE

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