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  1. Article ; Online: TNF-α signaling: TACE inhibition to put out the burning heart.

    Dittrich, Gesine M / Heineke, Joerg

    PLoS biology

    2020  Volume 18, Issue 12, Page(s) e3001037

    Abstract: More than 20 years ago, Seta and colleagues hypothesized that cytokines, which are activated by myocardial injury, significantly drive heart failure progression and would therefore be effective targets to treat cardiac dysfunction. Unfortunately, several ...

    Abstract More than 20 years ago, Seta and colleagues hypothesized that cytokines, which are activated by myocardial injury, significantly drive heart failure progression and would therefore be effective targets to treat cardiac dysfunction. Unfortunately, several clinical trials inhibiting key cytokines like tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (Il-1β) turned out negative or even revealed adverse clinical effects. Providing a potential mechanistic explanation for the ineffectiveness of TNF-α blockade in heart failure, novel findings demonstrate that the membrane-bound precursor form of TNF-α, transmembrane TNF-α (tmTNF-α), mediates cardioprotective effects during pressure overload-induced cardiac remodeling. This study suggests that preventing tmTNF-α cleavage by targeting the TNF-α converting enzyme (TACE) rather than inhibiting TNF-α signaling altogether might be a valuable therapeutic approach.
    MeSH term(s) ADAM17 Protein ; Cardiomegaly ; Humans ; Receptors, Tumor Necrosis Factor, Type II ; Signal Transduction ; Tumor Necrosis Factor-alpha
    Chemical Substances Receptors, Tumor Necrosis Factor, Type II ; Tumor Necrosis Factor-alpha ; ADAM17 Protein (EC 3.4.24.86)
    Language English
    Publishing date 2020-12-09
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2126776-5
    ISSN 1545-7885 ; 1544-9173
    ISSN (online) 1545-7885
    ISSN 1544-9173
    DOI 10.1371/journal.pbio.3001037
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Endothelial cells drive organ fibrosis in mice by inducing expression of the transcription factor SOX9.

    Trogisch, Felix A / Abouissa, Aya / Keles, Merve / Birke, Anne / Fuhrmann, Manuela / Dittrich, Gesine M / Weinzierl, Nina / Wink, Elvira / Cordero, Julio / Elsherbiny, Adel / Martin-Garrido, Abel / Grein, Steve / Hemanna, Shruthi / Hofmann, Ellen / Nicin, Luka / Bibli, Sofia-Iris / Airik, Rannar / Kispert, Andreas / Kist, Ralf /
    Quanchao, Sun / Kürschner, Sina W / Winkler, Manuel / Gretz, Norbert / Mogler, Carolin / Korff, Thomas / Koch, Philipp-Sebastian / Dimmeler, Stefanie / Dobreva, Gergana / Heineke, Joerg

    Science translational medicine

    2024  Volume 16, Issue 736, Page(s) eabq4581

    Abstract: Fibrosis is a hallmark of chronic disease. Although fibroblasts are involved, it is unclear to what extent endothelial cells also might contribute. We detected increased expression of the transcription ... ...

    Abstract Fibrosis is a hallmark of chronic disease. Although fibroblasts are involved, it is unclear to what extent endothelial cells also might contribute. We detected increased expression of the transcription factor
    MeSH term(s) Animals ; Humans ; Mice ; Disease Models, Animal ; Endothelial Cells ; Fibrosis ; Heart Failure ; Intercellular Signaling Peptides and Proteins ; Liver Cirrhosis/complications ; SOX9 Transcription Factor/genetics ; Transcription Factors
    Chemical Substances Intercellular Signaling Peptides and Proteins ; SOX9 protein, human ; SOX9 Transcription Factor ; Transcription Factors ; Sox9 protein, mouse
    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2518854-9
    ISSN 1946-6242 ; 1946-6234
    ISSN (online) 1946-6242
    ISSN 1946-6234
    DOI 10.1126/scitranslmed.abq4581
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis.

    Dittrich, Gesine M / Froese, Natali / Wang, Xue / Kroeger, Hannah / Wang, Honghui / Szaroszyk, Malgorzata / Malek-Mohammadi, Mona / Cordero, Julio / Keles, Merve / Korf-Klingebiel, Mortimer / Wollert, Kai C / Geffers, Robert / Mayr, Manuel / Conway, Simon J / Dobreva, Gergana / Bauersachs, Johann / Heineke, Joerg

    Basic research in cardiology

    2021  Volume 116, Issue 1, Page(s) 26

    Abstract: Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific ... ...

    Abstract Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling remain poorly understood. Cardiac fibroblasts express high levels of cardiogenic transcription factors such as GATA-4 and GATA-6, but their role in fibroblasts during stress is not known. Here, we show that fibroblast GATA-4 and GATA-6 promote adaptive remodeling in pressure overload induced cardiac hypertrophy. Using a mouse model with specific single or double deletion of Gata4 and Gata6 in stress activated fibroblasts, we found a reduced myocardial capillarization in mice with Gata4/6 double deletion following pressure overload, while single deletion of Gata4 or Gata6 had no effect. Importantly, we confirmed the reduced angiogenic response using an in vitro co-culture system with Gata4/6 deleted cardiac fibroblasts and endothelial cells. A comprehensive RNA-sequencing analysis revealed an upregulation of anti-angiogenic genes upon Gata4/6 deletion in fibroblasts, and siRNA mediated downregulation of these genes restored endothelial cell growth. In conclusion, we identified a novel role for the cardiogenic transcription factors GATA-4 and GATA-6 in heart fibroblasts, where both proteins act in concert to promote myocardial capillarization and heart function by directing intercellular crosstalk.
    MeSH term(s) Angiogenic Proteins/genetics ; Angiogenic Proteins/metabolism ; Animals ; Aorta/physiopathology ; Aorta/surgery ; Arterial Pressure ; Cardiomegaly/etiology ; Cardiomegaly/genetics ; Cardiomegaly/metabolism ; Cardiomegaly/physiopathology ; Cell Communication ; Cells, Cultured ; Constriction ; Disease Models, Animal ; Epithelial Cells/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology ; GATA4 Transcription Factor/genetics ; GATA4 Transcription Factor/metabolism ; GATA6 Transcription Factor/genetics ; GATA6 Transcription Factor/metabolism ; Heart Failure/etiology ; Heart Failure/genetics ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Humans ; Mice, Knockout ; Microvascular Density ; Myocardium/metabolism ; Myocardium/pathology ; Neovascularization, Physiologic ; Signal Transduction ; Ventricular Remodeling ; Mice
    Chemical Substances Angiogenic Proteins ; GATA4 Transcription Factor ; GATA6 Transcription Factor ; Gata4 protein, mouse ; Gata6 protein, mouse
    Language English
    Publishing date 2021-04-19
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-021-00862-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui IV Zs.30: Show issues Location:
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  4. Article ; Online: Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesis.

    Dittrich, Gesine M / Froese, Natali / Wang, Xue / Kroeger, Hannah / Wang, Honghui / Szaroszyk, Malgorzata / Malek-Mohammadi, Mona / Cordero, Julio / Keles, Merve / Korf-Klingebiel, Mortimer / Wollert, Kai C / Geffers, Robert / Mayr, Manuel / Conway, Simon J / Dobreva, Gergana / Bauersachs, Johann / Heineke, Joerg

    116 ; 1 ; 26 ; Basic research in cardiology ; United States ; Germany

    2021  

    Abstract: Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific ... ...

    Abstract Heart failure due to high blood pressure or ischemic injury remains a major problem for millions of patients worldwide. Despite enormous advances in deciphering the molecular mechanisms underlying heart failure progression, the cell-type specific adaptations and especially intercellular signaling remain poorly understood. Cardiac fibroblasts express high levels of cardiogenic transcription factors such as GATA-4 and GATA-6, but their role in fibroblasts during stress is not known. Here, we show that fibroblast GATA-4 and GATA-6 promote adaptive remodeling in pressure overload induced cardiac hypertrophy. Using a mouse model with specific single or double deletion of Gata4 and Gata6 in stress activated fibroblasts, we found a reduced myocardial capillarization in mice with Gata4/6 double deletion following pressure overload, while single deletion of Gata4 or Gata6 had no effect. Importantly, we confirmed the reduced angiogenic response using an in vitro co-culture system with Gata4/6 deleted cardiac fibroblasts and endothelial cells. A comprehensive RNA-sequencing analysis revealed an upregulation of anti-angiogenic genes upon Gata4/6 deletion in fibroblasts, and siRNA mediated downregulation of these genes restored endothelial cell growth. In conclusion, we identified a novel role for the cardiogenic transcription factors GATA-4 and GATA-6 in heart fibroblasts, where both proteins act in concert to promote myocardial capillarization and heart function by directing intercellular crosstalk.
    Keywords Angiogenesis ; Cardiac remodeling ; Fibroblast ; Intercellular crosstalk
    Subject code 610
    Language English
    Publishing date 2021-04-19
    Publisher Springer Nature
    Publishing country de
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Skeletal muscle derived Musclin protects the heart during pathological overload.

    Szaroszyk, Malgorzata / Kattih, Badder / Martin-Garrido, Abel / Trogisch, Felix A / Dittrich, Gesine M / Grund, Andrea / Abouissa, Aya / Derlin, Katja / Meier, Martin / Holler, Tim / Korf-Klingebiel, Mortimer / Völker, Katharina / Garfias Macedo, Tania / Pablo Tortola, Cristina / Boschmann, Michael / Huang, Nora / Froese, Natali / Zwadlo, Carolin / Malek Mohammadi, Mona /
    Luo, Xiaojing / Wagner, Michael / Cordero, Julio / Geffers, Robert / Batkai, Sandor / Thum, Thomas / Bork, Nadja / Nikolaev, Viacheslav O / Müller, Oliver J / Katus, Hugo A / El-Armouche, Ali / Kraft, Theresia / Springer, Jochen / Dobreva, Gergana / Wollert, Kai C / Fielitz, Jens / von Haehling, Stephan / Kuhn, Michaela / Bauersachs, Johann / Heineke, Joerg

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 149

    Abstract: Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from ... ...

    Abstract Cachexia is associated with poor prognosis in chronic heart failure patients, but the underlying mechanisms of cachexia triggered disease progression remain poorly understood. Here, we investigate whether the dysregulation of myokine expression from wasting skeletal muscle exaggerates heart failure. RNA sequencing from wasting skeletal muscles of mice with heart failure reveals a reduced expression of Ostn, which encodes the secreted myokine Musclin, previously implicated in the enhancement of natriuretic peptide signaling. By generating skeletal muscle specific Ostn knock-out and overexpressing mice, we demonstrate that reduced skeletal muscle Musclin levels exaggerate, while its overexpression in muscle attenuates cardiac dysfunction and myocardial fibrosis during pressure overload. Mechanistically, Musclin enhances the abundance of C-type natriuretic peptide (CNP), thereby promoting cardiomyocyte contractility through protein kinase A and inhibiting fibroblast activation through protein kinase G signaling. Because we also find reduced OSTN expression in skeletal muscle of heart failure patients, augmentation of Musclin might serve as therapeutic strategy.
    MeSH term(s) 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase/genetics ; 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase/metabolism ; Aged ; Aged, 80 and over ; Animals ; Cachexia/genetics ; Cachexia/metabolism ; Cachexia/physiopathology ; Cachexia/prevention & control ; Case-Control Studies ; Cyclic AMP-Dependent Protein Kinases/genetics ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Cyclic GMP-Dependent Protein Kinases/genetics ; Cyclic GMP-Dependent Protein Kinases/metabolism ; Disease Models, Animal ; Endomyocardial Fibrosis/genetics ; Endomyocardial Fibrosis/metabolism ; Endomyocardial Fibrosis/physiopathology ; Endomyocardial Fibrosis/prevention & control ; Female ; Gene Expression Regulation ; Heart Failure/genetics ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Heart Failure/prevention & control ; Heart Function Tests ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Proteins/agonists ; Muscle Proteins/antagonists & inhibitors ; Muscle Proteins/deficiency ; Muscle Proteins/genetics ; Muscle, Skeletal/metabolism ; Muscular Atrophy/genetics ; Muscular Atrophy/metabolism ; Muscular Atrophy/physiopathology ; Muscular Atrophy/prevention & control ; Myocardium/metabolism ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism ; Signal Transduction ; Transcription Factors/agonists ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/deficiency ; Transcription Factors/genetics
    Chemical Substances Muscle Proteins ; OSTN protein, human ; Ostn protein, mouse ; RNA, Small Interfering ; Transcription Factors ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Cyclic GMP-Dependent Protein Kinases (EC 2.7.11.12) ; 2',3'-Cyclic Nucleotide 3'-Phosphodiesterase (EC 3.1.4.37) ; Cnp protein, mouse (EC 3.1.4.37)
    Language English
    Publishing date 2022-01-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-021-27634-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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