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  1. AU="Atallah, Reham"
  2. AU="Schelhaas, Mart Jan"
  3. AU="Wang, Lixianqiu"
  4. AU="Cronin, Robert M"
  5. AU="Wu, Zhang Zhi"
  6. AU="Lombardo, Michael V" AU="Lombardo, Michael V"
  7. AU="Muhammad Asghar Pasha"
  8. AU="Linda Feketeová"
  9. AU="Aldrich, J Matthew"
  10. AU="Williams, Kristopher"
  11. AU="Calvet, Loreley"
  12. AU="Rui Pinto"
  13. AU="Feret, Geoff"
  14. AU="Sherrill-Mix, Scott"
  15. AU="Eleanor Eaton"
  16. AU="Latour, Corine H M"
  17. AU="Radetic, Mark"
  18. AU="James Jensen"
  19. AU="McFalls, Jeanne"
  20. AU="Sylvain Sebert"

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  1. Artikel ; Online: Dysregulation of metabolic pathways in pulmonary fibrosis.

    Rajesh, Rishi / Atallah, Reham / Bärnthaler, Thomas

    Pharmacology & therapeutics

    2023  Band 246, Seite(n) 108436

    Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disorder of unknown origin and the most common interstitial lung disease. It progresses with the recruitment of fibroblasts and myofibroblasts that contribute to the accumulation of ... ...

    Abstract Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disorder of unknown origin and the most common interstitial lung disease. It progresses with the recruitment of fibroblasts and myofibroblasts that contribute to the accumulation of extracellular matrix (ECM) proteins, leading to the loss of compliance and alveolar integrity, compromising the gas exchange capacity of the lung. Moreover, while there are therapeutics available, they do not offer a cure. Thus, there is a pressing need to identify better therapeutic targets. With the advent of transcriptomics, proteomics, and metabolomics, the cellular mechanisms underlying disease progression are better understood. Metabolic homeostasis is one such factor and its dysregulation has been shown to impact the outcome of IPF. Several metabolic pathways involved in the metabolism of lipids, protein and carbohydrates have been implicated in IPF. While metabolites are crucial for the generation of energy, it is now appreciated that metabolites have several non-metabolic roles in regulating cellular processes such as proliferation, signaling, and death among several other functions. Through this review, we succinctly elucidate the role of several metabolic pathways in IPF. Moreover, we also discuss potential therapeutics which target metabolism or metabolic pathways.
    Mesh-Begriff(e) Humans ; Lung/metabolism ; Idiopathic Pulmonary Fibrosis/pathology ; Fibroblasts/metabolism ; Myofibroblasts ; Metabolic Networks and Pathways ; Fibrosis
    Sprache Englisch
    Erscheinungsdatum 2023-05-05
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 194735-7
    ISSN 1879-016X ; 0163-7258
    ISSN (online) 1879-016X
    ISSN 0163-7258
    DOI 10.1016/j.pharmthera.2023.108436
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1183: Hefte anzeigen Standort:
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  2. Artikel: Succinate at the Crossroad of Metabolism and Angiogenesis: Roles of SDH, HIF1α and SUCNR1.

    Atallah, Reham / Olschewski, Andrea / Heinemann, Akos

    Biomedicines

    2022  Band 10, Heft 12

    Abstract: Angiogenesis is an essential process by which new blood vessels develop from existing ones. While adequate angiogenesis is a physiological process during, for example, tissue repair, insufficient and excessive angiogenesis stands on the pathological side. ...

    Abstract Angiogenesis is an essential process by which new blood vessels develop from existing ones. While adequate angiogenesis is a physiological process during, for example, tissue repair, insufficient and excessive angiogenesis stands on the pathological side. Fine balance between pro- and anti-angiogenic factors in the tissue environment regulates angiogenesis. Identification of these factors and how they function is a pressing topic to develop angiogenesis-targeted therapeutics. During the last decade, exciting data highlighted non-metabolic functions of intermediates of the mitochondrial Krebs cycle including succinate. Among these functions is the contribution of succinate to angiogenesis in various contexts and through different mechanisms. As the concept of targeting metabolism to treat a wide range of diseases is rising, in this review we summarize the mechanisms by which succinate regulates angiogenesis in normal and pathological settings. Gaining a comprehensive insight into how this metabolite functions as an angiogenic signal will provide a useful approach to understand diseases with aberrant or excessive angiogenic background, and may provide strategies to tackle them.
    Sprache Englisch
    Erscheinungsdatum 2022-12-01
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10123089
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: The JAK1/2 inhibitor baricitinib suppresses eosinophil effector function and restricts allergen-induced airway eosinophilia.

    Luschnig, Petra / Kienzl, Melanie / Roula, David / Pilic, Johannes / Atallah, Reham / Heinemann, Akos / Sturm, Eva M

    Biochemical pharmacology

    2021  Band 192, Seite(n) 114690

    Abstract: Background: Eosinophilic asthma is increasingly recognized as one of the most severe and difficult-to-treat asthma subtypes. The JAK/STAT pathway is the principal signaling mechanism for a variety of cytokines and growth factors involved in asthma. ... ...

    Abstract Background: Eosinophilic asthma is increasingly recognized as one of the most severe and difficult-to-treat asthma subtypes. The JAK/STAT pathway is the principal signaling mechanism for a variety of cytokines and growth factors involved in asthma. However, the direct effect of JAK inhibitors on eosinophil effector function has not been addressed thus far.
    Objective: Here we compared the effects of the JAK1/2 inhibitor baricitinib and the JAK3 inhibitor tofacitinib on eosinophil effector function in vitro and in vivo.
    Methods: Differentiation of murine bone marrow-derived eosinophils. Migratory responsiveness, respiratory burst, phagocytosis and apoptosis of human peripheral blood eosinophils were assessed in vitro. In vivo effects were investigated in a mouse model of acute house dust mite-induced airway inflammation in BALB/c mice.
    Results: Baricitinib more potently induced apoptosis and inhibited eosinophil chemotaxis and respiratory burst, while baricitinib and tofacitinib similarly affected eosinophil differentiation and phagocytosis. Of the JAK inhibitors, oral application of baricitinib more potently prevented lung eosinophilia in mice following allergen challenge. However, both JAK inhibitors neither affected airway resistance nor compliance.
    Conclusion: Our data suggest that the JAK1/2 inhibitor baricitinib is even more potent than the JAK3 inhibitor tofacitinib in suppressing eosinophil effector function. Thus, targeting the JAK1/2 pathway represents a promising therapeutic strategy for eosinophilic inflammation as observed in severe eosinophilic asthma.
    Mesh-Begriff(e) Adult ; Animals ; Azetidines/pharmacology ; Azetidines/therapeutic use ; Cells, Cultured ; Eosinophilia/chemically induced ; Eosinophilia/drug therapy ; Eosinophilia/immunology ; Eosinophils/drug effects ; Eosinophils/physiology ; Female ; Humans ; Janus Kinase 1/antagonists & inhibitors ; Janus Kinase 1/immunology ; Janus Kinase 2/antagonists & inhibitors ; Janus Kinase 2/immunology ; Janus Kinase Inhibitors/pharmacology ; Janus Kinase Inhibitors/therapeutic use ; Male ; Mice ; Mice, Inbred BALB C ; Purines/pharmacology ; Purines/therapeutic use ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Pyroglyphidae/immunology ; Sulfonamides/pharmacology ; Sulfonamides/therapeutic use ; Young Adult
    Chemische Substanzen Azetidines ; Janus Kinase Inhibitors ; Purines ; Pyrazoles ; Sulfonamides ; Janus Kinase 1 (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2) ; baricitinib (ISP4442I3Y)
    Sprache Englisch
    Erscheinungsdatum 2021-07-16
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2021.114690
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 19: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Artikel ; Online: Monocytes and Macrophages Serve as Potent Prostaglandin D

    Rittchen, Sonja / Jandl, Katharina / Lanz, Ilse / Reiter, Bernhard / Ferreirós, Nerea / Kratz, Daniel / Lindenmann, Jörg / Brcic, Luka / Bärnthaler, Thomas / Atallah, Reham / Olschewski, Horst / Sturm, Eva M / Heinemann, Akos

    International journal of molecular sciences

    2021  Band 22, Heft 21

    Abstract: Acute respiratory inflammation, most commonly resulting from bacterial or viral infection, is one of the leading causes of death and disability worldwide. The inflammatory lipid mediator prostaglandin ... ...

    Abstract Acute respiratory inflammation, most commonly resulting from bacterial or viral infection, is one of the leading causes of death and disability worldwide. The inflammatory lipid mediator prostaglandin D
    Mesh-Begriff(e) Acute Lung Injury/immunology ; Animals ; Humans ; Intramolecular Oxidoreductases/metabolism ; Lipocalins/metabolism ; Macrophages, Alveolar/metabolism ; Mice ; Monocytes/metabolism ; Prostaglandin D2/metabolism
    Chemische Substanzen Lipocalins ; Intramolecular Oxidoreductases (EC 5.3.-) ; prostaglandin R2 D-isomerase (EC 5.3.99.2) ; Prostaglandin D2 (RXY07S6CZ2)
    Sprache Englisch
    Erscheinungsdatum 2021-10-28
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222111697
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: SUCNR1 Is Expressed in Human Placenta and Mediates Angiogenesis: Significance in Gestational Diabetes.

    Atallah, Reham / Gindlhuber, Juergen / Platzer, Wolfgang / Bärnthaler, Thomas / Tatzl, Eva / Toller, Wolfgang / Strutz, Jasmin / Rittchen, Sonja / Luschnig, Petra / Birner-Gruenberger, Ruth / Wadsack, Christian / Heinemann, Akos

    International journal of molecular sciences

    2021  Band 22, Heft 21

    Abstract: Placental hypervascularization has been reported in pregnancy-related pathologies such as gestational diabetes mellitus (GDM). Nevertheless, the underlying causes behind this abnormality are not well understood. In this study, we addressed the expression ...

    Abstract Placental hypervascularization has been reported in pregnancy-related pathologies such as gestational diabetes mellitus (GDM). Nevertheless, the underlying causes behind this abnormality are not well understood. In this study, we addressed the expression of SUCNR1 (cognate succinate receptor) in human placental endothelial cells and hypothesized that the succinate-SUCNR1 axis might play a role in the placental hypervascularization reported in GDM. We measured significantly higher succinate levels in placental tissue lysates from women with GDM relative to matched controls. In parallel, SUCNR1 protein expression was upregulated in GDM tissue lysates as well as in isolated diabetic fetoplacental arterial endothelial cells (FpECAds). A positive correlation of SUCNR1 and vascular endothelial growth factor (VEGF) protein levels in tissue lysates indicated a potential link between the succinate-SUCNR1 axis and placental angiogenesis. In our in vitro experiments, succinate prompted hallmarks of angiogenesis in human umbilical vein endothelial cells (HUVECs) such as proliferation, migration and spheroid sprouting. These results were further validated in fetoplacental arterial endothelial cells (FpECAs), where succinate induced endothelial tube formation. VEGF gene expression was increased in response to succinate in both HUVECs and FpECAs. Yet, knockdown of SUCNR1 in HUVECs led to suppression of VEGF gene expression and abrogated the migratory ability and wound healing in response to succinate. In conclusion, our data underline SUCNR1 as a promising metabolic target in human placenta and as a potential driver of enhanced placental angiogenesis in GDM.
    Mesh-Begriff(e) Adult ; Case-Control Studies ; Cells, Cultured ; Diabetes, Gestational/genetics ; Diabetes, Gestational/metabolism ; Diabetes, Gestational/physiopathology ; Endothelium, Vascular/metabolism ; Female ; Human Umbilical Vein Endothelial Cells ; Humans ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Neovascularization, Physiologic/genetics ; Placenta/blood supply ; Placenta/metabolism ; Pregnancy ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Receptors, G-Protein-Coupled/physiology
    Chemische Substanzen Receptors, G-Protein-Coupled ; SUCNR1 protein, human
    Sprache Englisch
    Erscheinungsdatum 2021-11-07
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms222112048
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Prostaglandin D

    Rittchen, Sonja / Rohrer, Kathrin / Platzer, Wolfgang / Knuplez, Eva / Bärnthaler, Thomas / Marsh, Leigh M / Atallah, Reham / Sinn, Katharina / Klepetko, Walter / Sharma, Neha / Nagaraj, Chandran / Heinemann, Akos

    Biochemical pharmacology

    2020  Band 182, Seite(n) 114277

    Abstract: Life-threatening inflammatory conditions such as acute respiratory distress syndrome or sepsis often go hand in hand with severe vascular leakage. During inflammation, endothelial cell integrity and intact barrier function are crucial to limit leukocyte ... ...

    Abstract Life-threatening inflammatory conditions such as acute respiratory distress syndrome or sepsis often go hand in hand with severe vascular leakage. During inflammation, endothelial cell integrity and intact barrier function are crucial to limit leukocyte and plasma extravasation. Prostaglandin D
    Mesh-Begriff(e) Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Humans ; Microvessels/drug effects ; Microvessels/metabolism ; Prostaglandin D2/pharmacology ; Receptors, Prostaglandin E, EP4 Subtype/metabolism ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism
    Chemische Substanzen Receptors, Prostaglandin E, EP4 Subtype ; Prostaglandin D2 (RXY07S6CZ2)
    Sprache Englisch
    Erscheinungsdatum 2020-10-08
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2020.114277
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 19: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

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