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  1. Article ; Online: Progress in the mechanism and targeted drug therapy for COPD.

    Wang, Cuixue / Zhou, Jiedong / Wang, Jinquan / Li, Shujing / Fukunaga, Atsushi / Yodoi, Junji / Tian, Hai

    Signal transduction and targeted therapy

    2020  Volume 5, Issue 1, Page(s) 248

    Abstract: ... mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed ... immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and ... on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease ...

    Abstract Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, have significant therapeutic effects; however, they also cause side effects, including infection and immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. The mechanism by which Trx affects COPD is different from glucocorticoid-based mechanisms which regulate the inflammatory reaction in association with suppressing immune responses. In addition, Trx also improves the insensitivity of COPD to steroids by inhibiting the production and internalisation of macrophage migration inhibitory factor (MIF). Taken together, these findings suggest that Trx may be the ideal drug for treating COPD.
    MeSH term(s) Cyclic AMP-Dependent Protein Kinases/metabolism ; Cytokines/metabolism ; Drug Delivery Systems ; Humans ; MAP Kinase Signaling System/drug effects ; Oxidation-Reduction/drug effects ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/metabolism ; Thioredoxins/metabolism
    Chemical Substances Cytokines ; Thioredoxins (52500-60-4) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Keywords covid19
    Language English
    Publishing date 2020-10-27
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2886872-9
    ISSN 2059-3635 ; 2095-9907
    ISSN (online) 2059-3635
    ISSN 2095-9907
    DOI 10.1038/s41392-020-00345-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Progress in the mechanism and targeted drug therapy for COPD

    Cuixue Wang / Jiedong Zhou / Jinquan Wang / Shujing Li / Atsushi Fukunaga / Junji Yodoi / Hai Tian

    Signal Transduction and Targeted Therapy, Vol 5, Iss 1, Pp 1-

    2020  Volume 20

    Abstract: ... mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed ... immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and ... on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease ...

    Abstract Abstract Chronic obstructive pulmonary disease (COPD) is emphysema and/or chronic bronchitis characterised by long-term breathing problems and poor airflow. The prevalence of COPD has increased over the last decade and the drugs most commonly used to treat it, such as glucocorticoids and bronchodilators, have significant therapeutic effects; however, they also cause side effects, including infection and immunosuppression. Here we reviewed the pathogenesis and progression of COPD and elaborated on the effects and mechanisms of newly developed molecular targeted COPD therapeutic drugs. Among these new drugs, we focussed on thioredoxin (Trx). Trx effectively prevents the progression of COPD by regulating redox status and protease/anti-protease balance, blocking the NF-κB and MAPK signalling pathways, suppressing the activation and migration of inflammatory cells and the production of cytokines, inhibiting the synthesis and the activation of adhesion factors and growth factors, and controlling the cAMP-PKA and PI3K/Akt signalling pathways. The mechanism by which Trx affects COPD is different from glucocorticoid-based mechanisms which regulate the inflammatory reaction in association with suppressing immune responses. In addition, Trx also improves the insensitivity of COPD to steroids by inhibiting the production and internalisation of macrophage migration inhibitory factor (MIF). Taken together, these findings suggest that Trx may be the ideal drug for treating COPD.
    Keywords Medicine ; R ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article: [Progress in platelets and chronic obstructive pulmonary disease].

    Liang, L S / Mo, Y / Zhang, Z Y / Liang, P S / Xu, Pusheng

    Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases

    2022  Volume 45, Issue 10, Page(s) 1050–1054

    Abstract: ... Platelets inhibition may be an emerging therapeutic target for COPD, and antiplatelet therapy is expected to become ... the association between thrombocytosis and COPD. Platelets activation interacts with COPD. Antiplatelet therapy ... an inexpensive and effective treatment for COPD. This article reviewed the research progress in platelets and ...

    Abstract Platelets-related pathophysiological mechanism and clinical research is one of the research hot topics in chronic obstructive pulmonary disease (COPD) at home and abroad. Increasing evidence has proved the association between thrombocytosis and COPD. Platelets activation interacts with COPD. Antiplatelet therapy has been shown to have significant effects on both short-term and long-term outcomes in COPD. Platelets inhibition may be an emerging therapeutic target for COPD, and antiplatelet therapy is expected to become an inexpensive and effective treatment for COPD. This article reviewed the research progress in platelets and COPD.
    MeSH term(s) Blood Platelets ; Humans ; Platelet Aggregation Inhibitors/pharmacology ; Platelet Aggregation Inhibitors/therapeutic use ; Pulmonary Disease, Chronic Obstructive/drug therapy
    Chemical Substances Platelet Aggregation Inhibitors
    Language Chinese
    Publishing date 2022-10-07
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 1027965-9
    ISSN 1001-0939
    ISSN 1001-0939
    DOI 10.3760/cma.j.cn112147-20220425-00349
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 2465: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Dexmedetomidine targets miR-146a and participates in the progress of chronic obstructive pulmonary disease in vivo and in vitro.

    Li, Na / Li, Shuangfeng / Wu, Yehua / Xiong, Lu / Li, Tiejun / Xing, Dandan / Li, Qiuchang / Wu, Duozhi

    Genes & genomics

    2021  Volume 43, Issue 12, Page(s) 1371–1379

    Abstract: ... found.: Objective: To explore the role and mechanism of dexmedetomidine in COPD, and to provide ... of dexmedetomidine on the progression of COPD. The levels of IL-6, IL-1β and TNF-α in serum were measured by ELISA ... Background: Chronic obstructive pulmonary disease (COPD) is a chronic lung disease and the third ...

    Abstract Background: Chronic obstructive pulmonary disease (COPD) is a chronic lung disease and the third leading cause of death in the world. Dexmedetomidine has been reported to effectively inhibit histamine-induced bronchoconstriction. However, the molecular mechanism of dexmedetomidine in COPD has not been found.
    Objective: To explore the role and mechanism of dexmedetomidine in COPD, and to provide theoretical basis for clinical treatment of COPD.
    Methods: The expression of miR-146a was regulated by mimics or inhibitor and the relative expression of apoptotic proteins p53, Bax and Bcl-2 in human bronchial epithelial 16HBE cells was determined by real-time PCR and Western blot. Dexmedetomidine was treated for 16HBE cells and alveolar epithelial type II cells (AEC2), the cell apoptosis was detected by TUNEL and Hoechst33342 staining. A COPD rat model was established by smoking to test the effects of dexmedetomidine on the progression of COPD. The levels of IL-6, IL-1β and TNF-α in serum were measured by ELISA and the protein concentration of bronchoalveolar lavage fluid (BALF) was also detected in dexmedetomidine treated COPD rat model.
    Results: miR-146a promoted 16HBE cell apoptosis and reduced cell proliferation. Additionally, dexmedetomidine was showed to reduce the 16HBEL cell apoptosis through reducing the expression of miR-146a. Moreover, dexmedetomidine regulated cell apoptosis and cell apoptosis through miR-146a in AEC2 cells. More importantly, dexmedetomidine attenuated the morphology and pathology of COPD rat model.
    Conclusion: Dexmedetomidine reduced 16HBE cells and AEC2 cell apoptosis and attenuated COPD by down-regulating miR-146a.
    MeSH term(s) Animals ; Apoptosis ; Cell Line ; Cell Proliferation ; Cells, Cultured ; Dexmedetomidine/pharmacology ; Dexmedetomidine/therapeutic use ; Humans ; Interleukin-1beta/genetics ; Interleukin-1beta/metabolism ; Interleukin-6/genetics ; Interleukin-6/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/metabolism ; Rats ; Rats, Sprague-Dawley ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Interleukin-1beta ; Interleukin-6 ; MIRN146 microRNA, human ; MicroRNAs ; Tumor Necrosis Factor-alpha ; Dexmedetomidine (67VB76HONO)
    Language English
    Publishing date 2021-01-22
    Publishing country Korea (South)
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2504587-8
    ISSN 2092-9293 ; 1976-9571
    ISSN (online) 2092-9293
    ISSN 1976-9571
    DOI 10.1007/s13258-020-01019-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Current concepts in targeting chronic obstructive pulmonary disease pharmacotherapy: making progress towards personalised management.

    Woodruff, Prescott G / Agusti, Alvar / Roche, Nicolas / Singh, Dave / Martinez, Fernando J

    Lancet (London, England)

    2013  Volume 385, Issue 9979, Page(s) 1789–1798

    Abstract: Chronic obstructive pulmonary disease (COPD) is a common, complex, and heterogeneous disorder ... the underlying endotype. A few series of potential COPD endotypes and biomarkers have been suggested. Empirical ... knowledge will be gained from proof-of-concept trials in COPD with emerging drugs that target specific ...

    Abstract Chronic obstructive pulmonary disease (COPD) is a common, complex, and heterogeneous disorder that is responsible for substantial and growing morbidity, mortality, and health-care expense worldwide. Of imperative importance to decipher the complexity of COPD is to identify groups of patients with similar clinical characteristics, prognosis, or therapeutic needs, the so-called clinical phenotypes. This strategy is logical for research but might be of little clinical value because clinical phenotypes can overlap in the same patient and the same clinical phenotype could result from different biological mechanisms. With the goal to match assessment with treatment choices, the latest iteration of guidelines from the Global Initiative for Chronic Obstructive Lung Disease reorganised treatment objectives into two categories: to improve symptoms (ie, dyspnoea and health status) and to decrease future risk (as predicted by forced expiratory volume in 1 s level and exacerbations history). This change thus moves treatment closer to individualised medicine with available bronchodilators and anti-inflammatory drugs. Yet, future treatment options are likely to include targeting endotypes that represent subtypes of patients defined by a distinct pathophysiological mechanism. Specific biomarkers of these endotypes would be particularly useful in clinical practice, especially in patients in which clinical phenotype alone is insufficient to identify the underlying endotype. A few series of potential COPD endotypes and biomarkers have been suggested. Empirical knowledge will be gained from proof-of-concept trials in COPD with emerging drugs that target specific inflammatory pathways. In every instance, specific endotype and biomarker efforts will probably be needed for the success of these trials, because the pathways are likely to be operative in only a subset of patients. Network analysis of human diseases offers the possibility to improve understanding of disease pathobiological complexity and to help with the development of new treatment alternatives and, importantly, a reclassification of complex diseases. All these developments should pave the way towards personalised treatment of patients with COPD in the clinic.
    MeSH term(s) Biomarkers ; Disease Management ; Disease Progression ; Eosinophilia ; Evidence-Based Medicine ; Humans ; Inflammation ; Precision Medicine ; Pulmonary Disease, Chronic Obstructive/classification ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Th2 Cells ; alpha 1-Antitrypsin Deficiency
    Chemical Substances Biomarkers
    Language English
    Publishing date 2013-06-17
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 3306-6
    ISSN 1474-547X ; 0023-7507 ; 0140-6736
    ISSN (online) 1474-547X
    ISSN 0023-7507 ; 0140-6736
    DOI 10.1016/S0140-6736(15)60693-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.5: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Zs.MG 94: Show issues

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  6. Article ; Online: Protein phosphatase 2A (PP2A): a key phosphatase in the progression of chronic obstructive pulmonary disease (COPD) to lung cancer.

    Nader, Cassandra P / Cidem, Aylin / Verrills, Nicole M / Ammit, Alaina J

    Respiratory research

    2019  Volume 20, Issue 1, Page(s) 222

    Abstract: ... of tumour pathogenesis. Finally, we highlight PP2A as a druggable target in the treatment of COPD and LC and ... obstructive pulmonary disease (COPD). The molecular mechanisms that mediate chronic inflammation and lung function impairment ... in the progression of COPD to LC. In this review, we uncover the importance of the functional and active PP2A ...

    Abstract Lung cancer (LC) has the highest relative risk of development as a comorbidity of chronic obstructive pulmonary disease (COPD). The molecular mechanisms that mediate chronic inflammation and lung function impairment in COPD have been identified in LC. This suggests the two diseases are more linked than once thought. Emerging data in relation to a key phosphatase, protein phosphatase 2A (PP2A), and its regulatory role in inflammatory and tumour suppression in both disease settings suggests that it may be critical in the progression of COPD to LC. In this review, we uncover the importance of the functional and active PP2A holoenzyme in the context of both diseases. We describe PP2A inactivation via direct and indirect means and explore the actions of two key PP2A endogenous inhibitors, cancerous inhibitor of PP2A (CIP2A) and inhibitor 2 of PP2A (SET), and the role they play in COPD and LC. We explain how dysregulation of PP2A in COPD creates a favourable inflammatory micro-environment and promotes the initiation and progression of tumour pathogenesis. Finally, we highlight PP2A as a druggable target in the treatment of COPD and LC and demonstrate the potential of PP2A re-activation as a strategy to halt COPD disease progression to LC. Although further studies are required to elucidate if PP2A activity in COPD is a causal link for LC progression, studies focused on the potential of PP2A reactivating agents to reduce the risk of LC formation in COPD patients will be pivotal in improving clinical outcomes for both COPD and LC patients in the future.
    MeSH term(s) Animals ; Autoantigens/administration & dosage ; Disease Progression ; Humans ; Intracellular Signaling Peptides and Proteins/administration & dosage ; Lung Neoplasms/diagnosis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/enzymology ; Membrane Proteins/administration & dosage ; Protein Phosphatase 2/antagonists & inhibitors ; Protein Phosphatase 2/metabolism ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/enzymology
    Chemical Substances Autoantigens ; CIP2A protein, human ; Intracellular Signaling Peptides and Proteins ; Membrane Proteins ; Protein Phosphatase 2 (EC 3.1.3.16)
    Language English
    Publishing date 2019-10-17
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2041675-1
    ISSN 1465-993X ; 1465-993X
    ISSN (online) 1465-993X
    ISSN 1465-993X
    DOI 10.1186/s12931-019-1192-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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