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  1. Article ; Online: Circulating miRNAs in Hypertrophic Cardiomyopathy: A Long and Bumpy Road.

    van der Meer, Peter / Van Linthout, Sophie

    Circulation. Heart failure

    2023  Volume 16, Issue 6, Page(s) e010694

    MeSH term(s) Humans ; Heart Failure ; Cardiomyopathy, Hypertrophic/genetics ; MicroRNAs/genetics
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2023-06-12
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2429459-7
    ISSN 1941-3297 ; 1941-3289
    ISSN (online) 1941-3297
    ISSN 1941-3289
    DOI 10.1161/CIRCHEARTFAILURE.123.010694
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6745: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Immuno-cardio-oncology: Killing two birds with one stone?

    Van Linthout, Sophie / Volk, Hans-Dieter

    Frontiers in immunology

    2022  Volume 13, Page(s) 1018772

    Abstract: Inflammation and a dysregulated immune system are common denominators of cancer and cardiovascular disease (CVD). Immuno-cardio-oncology addresses the interconnected immunological aspect in both cancer and CVD and the integration of immunotherapies and ... ...

    Abstract Inflammation and a dysregulated immune system are common denominators of cancer and cardiovascular disease (CVD). Immuno-cardio-oncology addresses the interconnected immunological aspect in both cancer and CVD and the integration of immunotherapies and anti-inflammatory therapies in both distinct disease entities. Building on prominent examples of convergent inflammation (IL-1ß biology) and immune disbalance (CD20 cells) in cancer and CVD/heart failure, the review tackles both the roadblocks and opportunities of repurposed use of IL-1ß drugs and anti-CD20 antibodies in both fields, and discusses the use of advanced therapies e.g. chimeric antigen receptor (CAR) T cells, that can address the raising burden of both cancer and CVD. Finally, it is discussed how inspired by precision medicine in oncology, the use of biomarker-driven patient stratification is needed to better guide anti-inflammatory/immunomodulatory therapeutic interventions in cardiology.
    MeSH term(s) Humans ; Medical Oncology ; Heart ; Immunotherapy ; Cardiovascular Diseases/therapy ; Inflammation
    Language English
    Publishing date 2022-11-17
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.1018772
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model.

    Pappritz, Kathleen / Van Linthout, Sophie

    Biology

    2020  Volume 9, Issue 10

    Abstract: Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The ...

    Abstract Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The pathogenesis of viral myocarditis is conceptually a multiphase process, initiated by the infection of cardiomyocytes, followed by activation of the immune system, and resulting in myocardial fibrosis and left ventricular dysfunction. In parallel to the direct infection of the heart, CVB3 replicates in lymphatic organs such as the pancreas. Due to infection of the pancreas, the model of experimental CVB3-induced myocarditis is estimated as a severe burden for the challenged animals. Application of analgesics in frame of the animal welfare act (European directive 2010/63/EU) is more and more becoming a matter of debate. For this purpose, we summarized published studies for 13 different opioids and discussed their potential impact on CVB3-induced myocarditis. In addition, with this summary we also want to provide guidance for researchers beyond the myocarditis field to estimate the impact of opioids on the immune system for their specific model. In the literature, both immunosuppressive as well as immune-activating effects of opioids have been described, but examinations in experimental CVB3-induced myocarditis have still not been reported so far. Based on the existing publications, administration of opioids in experimental CVB3-induced myocarditis might result in more severe disease progression, including higher mortality, or a less pronounced myocarditis model, failing to be used for the establishment of new treatment options. Taken together, the applicability of opioids in experimental CVB3-induced myocarditis and in inflammatory models in general needs to be carefully evaluated and further investigated.
    Language English
    Publishing date 2020-10-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology9100335
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Left ventricle- and skeletal muscle-derived fibroblasts exhibit a differential inflammatory and metabolic responsiveness to interleukin-6.

    Matz, Isabell / Pappritz, Kathleen / Springer, Jochen / Van Linthout, Sophie

    Frontiers in immunology

    2022  Volume 13, Page(s) 947267

    Abstract: Interleukin-6 (IL-6) is an important player in chronic inflammation associated with heart failure and tumor-induced cachexia. Fibroblasts are salient mediators of both inflammation and fibrosis. Whereas the general outcome of IL-6 on the heart's function ...

    Abstract Interleukin-6 (IL-6) is an important player in chronic inflammation associated with heart failure and tumor-induced cachexia. Fibroblasts are salient mediators of both inflammation and fibrosis. Whereas the general outcome of IL-6 on the heart's function and muscle wasting has been intensively studied, the influence of IL-6 on fibroblasts of the heart and skeletal muscle (SM) has not been analyzed so far. We illustrate that SM-derived fibroblasts exhibit higher basal mRNA expression of α-SMA, extracellular matrix molecules (collagen1a1/3a1/5a1), and chemokines (CCL2, CCL7, and CX3CL1) as compared to the left ventricle (LV)-derived fibroblasts. IL-6 drives the transdifferentiation of fibroblasts into myofibroblasts as indicated by an increase in α-SMA expression and upregulates NLRP3 inflammasome activity in both LV- and SM-derived fibroblasts. IL-6 increases the release of CCL7 to CX3CL1 in the supernatant of SM-derived fibroblasts associated with the attraction of more pro(Ly6C
    MeSH term(s) Fibroblasts/metabolism ; Heart Ventricles/metabolism ; Humans ; Inflammation/metabolism ; Interleukin-6/metabolism ; Muscle, Skeletal/metabolism
    Chemical Substances IL6 protein, human ; Interleukin-6
    Language English
    Publishing date 2022-07-28
    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.2022.947267
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Lost in markers? Time for phenomics and phenomapping in dilated cardiomyopathy.

    Van Linthout, Sophie / Tschöpe, Carsten

    European journal of heart failure

    2017  Volume 19, Issue 4, Page(s) 499–501

    Language English
    Publishing date 2017-04
    Publishing country England
    Document type Editorial
    ZDB-ID 1483672-5
    ISSN 1879-0844 ; 1388-9842
    ISSN (online) 1879-0844
    ISSN 1388-9842
    DOI 10.1002/ejhf.744
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5299: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: SARS-CoV-2-related myocarditis-like syndromes Shakespeare's question: what's in a name?

    Van Linthout, Sophie / Klingel, Karin / Tschöpe, Carsten

    European journal of heart failure

    2020  Volume 22, Issue 6, Page(s) 922–925

    MeSH term(s) Betacoronavirus ; COVID-19 ; Coronavirus ; Coronavirus Infections ; Heart Failure ; Humans ; Myocarditis ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2 ; Shock, Cardiogenic ; Syndrome
    Keywords covid19
    Language English
    Publishing date 2020-06-20
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 1483672-5
    ISSN 1879-0844 ; 1388-9842
    ISSN (online) 1879-0844
    ISSN 1388-9842
    DOI 10.1002/ejhf.1899
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5299: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: The Quest for Antiinflammatory and Immunomodulatory Strategies in Heart Failure.

    Van Linthout, Sophie / Tschöpe, Carsten

    Clinical pharmacology and therapeutics

    2019  Volume 106, Issue 6, Page(s) 1198–1208

    Abstract: Intensive research over the last 3 decades has unequivocally demonstrated the relevance of inflammation in heart failure (HF). Despite our current and ever increasing knowledge about inflammation, the clinical success of antiinflammatory and ... ...

    Abstract Intensive research over the last 3 decades has unequivocally demonstrated the relevance of inflammation in heart failure (HF). Despite our current and ever increasing knowledge about inflammation, the clinical success of antiinflammatory and immunomodulatory therapies in HF is still limited. This review outlines the complexity and diversity of inflammation, its reciprocal interaction with HF, and addresses future perspectives, calling for immunomodulatory therapies that are specific for factors that activate the immune system without the risk of nonspecific immune suppression.
    MeSH term(s) Adrenergic beta-Antagonists/therapeutic use ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Anti-Inflammatory Agents/therapeutic use ; Atherosclerosis/immunology ; Calgranulin A/antagonists & inhibitors ; Calgranulin B ; Cytokines/immunology ; Drug Development ; Heart Failure/immunology ; Heart Failure/therapy ; Humans ; Immunologic Factors/therapeutic use ; Inflammation/immunology ; Mesenchymal Stem Cell Transplantation ; Methotrexate/therapeutic use ; NLR Family, Pyrin Domain-Containing 3 Protein/antagonists & inhibitors ; T-Lymphocytes, Regulatory ; Tumor Necrosis Factor Inhibitors/adverse effects ; Tumor Necrosis Factor-alpha/immunology
    Chemical Substances Adrenergic beta-Antagonists ; Angiotensin-Converting Enzyme Inhibitors ; Anti-Inflammatory Agents ; Calgranulin A ; Calgranulin B ; Cytokines ; Immunologic Factors ; NLR Family, Pyrin Domain-Containing 3 Protein ; Tumor Necrosis Factor Inhibitors ; Tumor Necrosis Factor-alpha ; Methotrexate (YL5FZ2Y5U1)
    Language English
    Publishing date 2019-10-28
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 123793-7
    ISSN 1532-6535 ; 0009-9236
    ISSN (online) 1532-6535
    ISSN 0009-9236
    DOI 10.1002/cpt.1637
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 20: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: A Toolbox of Potential Immune-Related Therapies for Inflammatory Cardiomyopathy.

    Elsanhoury, Ahmed / Tschöpe, Carsten / Van Linthout, Sophie

    Journal of cardiovascular translational research

    2020  Volume 14, Issue 1, Page(s) 75–87

    Abstract: Myocarditis is a multifactorial disorder, characterized by an inflammatory reaction in the myocardium, predominantly triggered by infectious agents, but also by antigen mimicry or autoimmunity in susceptible individuals. Unless spontaneously resolved, a ... ...

    Abstract Myocarditis is a multifactorial disorder, characterized by an inflammatory reaction in the myocardium, predominantly triggered by infectious agents, but also by antigen mimicry or autoimmunity in susceptible individuals. Unless spontaneously resolved, a chronic inflammatory course concludes with cardiac muscle dysfunction portrayed by ventricular dilatation, clinically termed inflammatory cardiomyopathy (Infl-CM). Treatment strategies aim to resolve chronic inflammation and preserve cardiac function. Beside standard heart failure treatments, which only play a supportive role in this condition, systemic immunosuppressants are used to diminish inflammatory cell function at the cost of noxious side effects. To date, the treatment protocols are expert-based without large clinical evidence. This review describes concept and contemporary strategies to alleviate myocardial inflammation and sheds light on potential inflammatory targets in an evidence-based order.
    MeSH term(s) Autoimmunity ; Cardiomyopathies/drug therapy ; Cardiomyopathies/immunology ; Humans ; Immunosuppressive Agents/therapeutic use ; Inflammation/drug therapy ; Inflammation/immunology ; Myocardium/immunology
    Chemical Substances Immunosuppressive Agents
    Language English
    Publishing date 2020-05-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2422411-X
    ISSN 1937-5395 ; 1937-5387
    ISSN (online) 1937-5395
    ISSN 1937-5387
    DOI 10.1007/s12265-020-10025-4
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  9. Article ; Online: Opioid-Induced Immunomodulation

    Kathleen Pappritz / Sophie Van Linthout

    Biology, Vol 9, Iss 335, p

    Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

    2020  Volume 335

    Abstract: Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The ...

    Abstract Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The pathogenesis of viral myocarditis is conceptually a multiphase process, initiated by the infection of cardiomyocytes, followed by activation of the immune system, and resulting in myocardial fibrosis and left ventricular dysfunction. In parallel to the direct infection of the heart, CVB3 replicates in lymphatic organs such as the pancreas. Due to infection of the pancreas, the model of experimental CVB3-induced myocarditis is estimated as a severe burden for the challenged animals. Application of analgesics in frame of the animal welfare act (European directive 2010/63/EU) is more and more becoming a matter of debate. For this purpose, we summarized published studies for 13 different opioids and discussed their potential impact on CVB3-induced myocarditis. In addition, with this summary we also want to provide guidance for researchers beyond the myocarditis field to estimate the impact of opioids on the immune system for their specific model. In the literature, both immunosuppressive as well as immune-activating effects of opioids have been described, but examinations in experimental CVB3-induced myocarditis have still not been reported so far. Based on the existing publications, administration of opioids in experimental CVB3-induced myocarditis might result in more severe disease progression, including higher mortality, or a less pronounced myocarditis model, failing to be used for the establishment of new treatment options. Taken together, the applicability of opioids in experimental CVB3-induced myocarditis and in inflammatory models in general needs to be carefully evaluated and further investigated.
    Keywords Coxsackievirus B3 (CVB3)-induced myocarditis ; opioids ; immunomodulation ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Coronary microvascular dysfunction in heart failure with preserved ejection fraction - adding new pieces to the jigsaw puzzle.

    Van Linthout, Sophie / Rimoldi, Ornella / Tschöpe, Carsten / Camici, Paolo G

    European journal of heart failure

    2020  Volume 22, Issue 3, Page(s) 442–444

    MeSH term(s) Endothelium ; Heart Failure ; Humans ; Stroke Volume ; Ventricular Dysfunction, Left ; Ventricular Function, Left
    Language English
    Publishing date 2020-01-07
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 1483672-5
    ISSN 1879-0844 ; 1388-9842
    ISSN (online) 1879-0844
    ISSN 1388-9842
    DOI 10.1002/ejhf.1720
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5299: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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