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  1. Artikel ; Online: Pectins from various sources inhibit galectin-3-related cardiac fibrosis.

    Pozder Geb Gehlken, Carolin / Rogier van der Velde, A / Meijers, Wouter C / Silljé, Herman H W / Muntendam, Pieter / Dokter, Martin M / van Gilst, Wiek H / Schols, Henk A / de Boer, Rudolf A

    Current research in translational medicine

    2021  Band 70, Heft 1, Seite(n) 103321

    Abstract: Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with ... ...

    Abstract Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with the strongest galectin-3 inhibitory capacity. We evaluated the in vitro inhibitory capacity, identified potent pectins, and tested if this potency could be validated in a mouse model of myocardial fibrosis.
    Methods: Various pectin fractions were screened in vitro. Modified rhubarb pectin (EMRP) was identified as the most potent inhibitor of galectin-3 and compared to the well-known modified citrus pectin (MCP). Our findings were validated in a mouse model of myocardial fibrosis, which was induced by angiotensin II (Ang II) infusion.
    Results: Ang II infusion was associated with a 4-5-fold increase in fibrosis signal in the tissue of the left ventricle, compared to the control group (0•22±0•10 to 1•08±0•53%; P < 0•001). After treatment with rhubarb pectin, fibrosis was reduced by 57% vs. Ang II alone while this reduction was 30% with the well-known MCP (P = NS, P < 0•05). Treatment was associated with a reduced cardiac inflammatory response and preserved cardiac function.
    Conclusion: The galectin-3 inhibitor natural rhubarb pectin has a superior inhibitory capacity over established pectins, substantially attenuates cardiac fibrosis, and preserves cardiac function in vivo. Bioactive pectins are natural sources of galectin-3 inhibitors and may be helpful in the prevention of heart failure or other diseases characterized by fibrosis.
    Funding: Dr. Meijers is supported by the Mandema-Stipendium of the Junior Scientific Masterclass 2020-10, University Medical Center Groningen and by the Netherlands Heart Foundation (Dekkerbeurs 2021)Dr. de Boer is supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21; CVON RED-CVD, grant 2017-11; CVON PREDICT2, grant 2018-30; and CVON DOUBLE DOSE, grant 2020B005), by a grant from the leDucq Foundation (Cure PhosphoLambaN induced Cardiomyopathy (Cure-PLaN), and by a grant from the European Research Council (ERC CoG 818715, SECRETE-HF).
    Mesh-Begriff(e) Animals ; Disease Models, Animal ; Fibrosis ; Galectin 3 ; Mice ; Pectins
    Chemische Substanzen Galectin 3 ; Pectins (89NA02M4RX)
    Sprache Englisch
    Erscheinungsdatum 2021-11-23
    Erscheinungsland France
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2452-3186
    ISSN (online) 2452-3186
    DOI 10.1016/j.retram.2021.103321
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Pectins from various sources inhibit galectin-3-related cardiac fibrosis

    Pozder geb. Gehlken, Carolin / Rogier van der Velde, A. / Meijers, Wouter C. / Silljé, Herman H.W. / Muntendam, Pieter / Dokter, Martin M. / van Gilst, Wiek H. / Schols, Henk A. / de Boer, Rudolf A.

    Current Research in Translational Medicine

    2022  Band 70, Heft 1

    Abstract: Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with ... ...

    Abstract Purpose of the study: A major challenge in cardiology remains in finding a therapy for cardiac fibrosis. Inhibition of galectin-3 with pectins attenuates fibrosis in animal models of heart failure. The purpose of this study is to identify pectins with the strongest galectin-3 inhibitory capacity. We evaluated the in vitro inhibitory capacity, identified potent pectins, and tested if this potency could be validated in a mouse model of myocardial fibrosis. Methods: Various pectin fractions were screened in vitro. Modified rhubarb pectin (EMRP) was identified as the most potent inhibitor of galectin-3 and compared to the well-known modified citrus pectin (MCP). Our findings were validated in a mouse model of myocardial fibrosis, which was induced by angiotensin II (Ang II) infusion. Results: Ang II infusion was associated with a 4–5-fold increase in fibrosis signal in the tissue of the left ventricle, compared to the control group (0•22±0•10 to 1•08±0•53%; P < 0•001). After treatment with rhubarb pectin, fibrosis was reduced by 57% vs. Ang II alone while this reduction was 30% with the well-known MCP (P = NS, P < 0•05). Treatment was associated with a reduced cardiac inflammatory response and preserved cardiac function. Conclusion: The galectin-3 inhibitor natural rhubarb pectin has a superior inhibitory capacity over established pectins, substantially attenuates cardiac fibrosis, and preserves cardiac function in vivo. Bioactive pectins are natural sources of galectin-3 inhibitors and may be helpful in the prevention of heart failure or other diseases characterized by fibrosis. Funding: Dr. Meijers is supported by the Mandema-Stipendium of the Junior Scientific Masterclass 2020-10, University Medical Center Groningen and by the Netherlands Heart Foundation (Dekkerbeurs 2021)Dr. de Boer is supported by the Netherlands Heart Foundation (CVON SHE-PREDICTS-HF, grant 2017-21; CVON RED-CVD, grant 2017-11; CVON PREDICT2, grant 2018-30; and CVON DOUBLE DOSE, grant 2020B005), by a grant from the leDucq Foundation ...
    Schlagwörter Affinity ; Fibrosis ; Galectin-3 ; Heart failure ; Inhibitor ; Pectin
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsland nl
    Dokumenttyp Artikel ; Online
    ISSN 2452-3186
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Galectin-3 and heart failure: prognosis, prediction & clinical utility.

    Filipe, Mando D / Meijers, Wouter C / Rogier van der Velde, A / de Boer, Rudolf A

    Clinica chimica acta; international journal of clinical chemistry

    2014  Band 443, Seite(n) 48–56

    Abstract: Heart failure (HF) is a leading cause of mortality in the western world. Despite advances in the treatment of HF, like the use of angiotensin-converting enzyme (ACE) inhibitors, β-blockers, angiotensin receptor blockers (ARBs), mineralocorticoid receptor ...

    Abstract Heart failure (HF) is a leading cause of mortality in the western world. Despite advances in the treatment of HF, like the use of angiotensin-converting enzyme (ACE) inhibitors, β-blockers, angiotensin receptor blockers (ARBs), mineralocorticoid receptor antagonists (MRAs), and implantable cardiac defibrillators, prognosis of HF patients remains poor. For clinicians dealing with HF patients, risk prediction in both acute, chronic, and new onset HF remains a challenge. Biomarkers might help in risk stratification and may guide the proper use of limited resources and therapy. Galectin-3 is an emerging biomarker which has been linked to tissue fibrosis, a hallmark in cardiac remodeling and HF. Galectin-3 can reliably be measured in the circulation, and several recent studies have shown the prognostic value of galectin-3 in acute and chronic HF, and its potential utility in the general population. The purpose of this review was to summarize the literature and explore the potential role of galectin-3 as a biomarker in HF.
    Mesh-Begriff(e) Biomarkers/analysis ; Galectin 3/analysis ; Heart Failure/diagnosis ; Heart Failure/metabolism ; Humans ; Prognosis
    Chemische Substanzen Biomarkers ; Galectin 3 ; LGALS3 protein, human
    Sprache Englisch
    Erscheinungsdatum 2014-10-18
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80228-1
    ISSN 1873-3492 ; 0009-8981
    ISSN (online) 1873-3492
    ISSN 0009-8981
    DOI 10.1016/j.cca.2014.10.009
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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