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  1. Article ; Online: Calpains in the cardiovascular system.

    Inserte, Javier

    Cardiovascular research

    2012  Volume 96, Issue 1, Page(s) 9–10

    MeSH term(s) Animals ; Calpain/metabolism ; Cardiovascular System/enzymology ; Humans
    Chemical Substances Calpain (EC 3.4.22.-)
    Language English
    Publishing date 2012-10-01
    Publishing country England
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvs245
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  2. Article ; Online: Long-Term Protective Effects of Succinate Dehydrogenase Inhibition during Reperfusion with Malonate on Post-Infarction Left Ventricular Scar and Remodeling in Mice.

    Valls-Lacalle, Laura / Consegal, Marta / Ganse, Freddy G / Yáñez-Bisbe, Laia / Pastor, Javier / Ruiz-Meana, Marisol / Inserte, Javier / Benito, Begoña / Ferreira-González, Ignacio / Rodríguez-Sinovas, Antonio

    International journal of molecular sciences

    2024  Volume 25, Issue 8

    Abstract: Succinate dehydrogenase inhibition with malonate during initial reperfusion reduces myocardial infarct size in both isolated mouse hearts subjected to global ischemia and in in situ pig hearts subjected to transient coronary ligature. However, the long- ... ...

    Abstract Succinate dehydrogenase inhibition with malonate during initial reperfusion reduces myocardial infarct size in both isolated mouse hearts subjected to global ischemia and in in situ pig hearts subjected to transient coronary ligature. However, the long-term effects of acute malonate treatment are unknown. Here, we investigated whether the protective effects of succinate dehydrogenase inhibition extend to a reduction in scar size and adverse left ventricular remodeling 28 days after myocardial infarction. Initially, ten wild-type mice were subjected to 45 min of left anterior descending coronary artery (LAD) occlusion, followed by 24 h of reperfusion, and were infused during the first 15 min of reperfusion with saline with or without disodium malonate (10 mg/kg/min, 120 μL/kg/min). Malonate-treated mice depicted a significant reduction in infarct size (15.47 ± 3.40% of area at risk vs. 29.34 ± 4.44% in control animals,
    MeSH term(s) Animals ; Malonates/pharmacology ; Myocardial Infarction/drug therapy ; Myocardial Infarction/pathology ; Mice ; Succinate Dehydrogenase/metabolism ; Succinate Dehydrogenase/antagonists & inhibitors ; Male ; Ventricular Remodeling/drug effects ; Myocardial Reperfusion Injury/drug therapy ; Myocardial Reperfusion Injury/pathology ; Cicatrix/pathology ; Cicatrix/drug therapy ; Mice, Inbred C57BL
    Chemical Substances Malonates ; Succinate Dehydrogenase (EC 1.3.99.1) ; malonic acid (9KX7ZMG0MK)
    Language English
    Publishing date 2024-04-15
    Publishing country Switzerland
    Document type 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/ijms25084366
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  3. Article ; Online: Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy.

    Aluja, David / Delgado-Tomás, Sara / Ruiz-Meana, Marisol / Barrabés, José A / Inserte, Javier

    International journal of molecular sciences

    2022  Volume 23, Issue 8

    Abstract: Despite advances in its treatment, heart failure remains a major cause of morbidity and mortality, evidencing an urgent need for novel mechanism-based targets and strategies. Myocardial hypertrophy, caused by a wide variety of chronic stress stimuli, ... ...

    Abstract Despite advances in its treatment, heart failure remains a major cause of morbidity and mortality, evidencing an urgent need for novel mechanism-based targets and strategies. Myocardial hypertrophy, caused by a wide variety of chronic stress stimuli, represents an independent risk factor for the development of heart failure, and its prevention constitutes a clinical objective. Recent studies performed in preclinical animal models support the contribution of the Ca
    MeSH term(s) Animals ; Calcium-Binding Proteins ; Calpain/metabolism ; Cardiomegaly/drug therapy ; Heart Failure/drug therapy
    Chemical Substances Calcium-Binding Proteins ; Calpain (EC 3.4.22.-)
    Language English
    Publishing date 2022-04-07
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms23084103
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  4. Article ; Online: Calpains as Potential Therapeutic Targets for Myocardial Hypertrophy

    David Aluja / Sara Delgado-Tomás / Marisol Ruiz-Meana / José A. Barrabés / Javier Inserte

    International Journal of Molecular Sciences, Vol 23, Iss 4103, p

    2022  Volume 4103

    Abstract: Despite advances in its treatment, heart failure remains a major cause of morbidity and mortality, evidencing an urgent need for novel mechanism-based targets and strategies. Myocardial hypertrophy, caused by a wide variety of chronic stress stimuli, ... ...

    Abstract Despite advances in its treatment, heart failure remains a major cause of morbidity and mortality, evidencing an urgent need for novel mechanism-based targets and strategies. Myocardial hypertrophy, caused by a wide variety of chronic stress stimuli, represents an independent risk factor for the development of heart failure, and its prevention constitutes a clinical objective. Recent studies performed in preclinical animal models support the contribution of the Ca 2+ -dependent cysteine proteases calpains in regulating the hypertrophic process and highlight the feasibility of their long-term inhibition as a pharmacological strategy. In this review, we discuss the existing evidence implicating calpains in the development of cardiac hypertrophy, as well as the latest advances in unraveling the underlying mechanisms. Finally, we provide an updated overview of calpain inhibitors that have been explored in preclinical models of cardiac hypertrophy and the progress made in developing new compounds that may serve for testing the efficacy of calpain inhibition in the treatment of pathological cardiac hypertrophy.
    Keywords calpain ; calpastatin ; myocardial hypertrophy ; heart failure ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2022-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: TRPV4 Channels Promote Pathological, but Not Physiological, Cardiac Remodeling through the Activation of Calcineurin/NFAT and TRPC6.

    Yáñez-Bisbe, Laia / Moya, Mar / Rodríguez-Sinovas, Antonio / Ruiz-Meana, Marisol / Inserte, Javier / Tajes, Marta / Batlle, Montserrat / Guasch, Eduard / Mas-Stachurska, Aleksandra / Miró, Elisabet / Rivas, Nuria / Ferreira González, Ignacio / Garcia-Elias, Anna / Benito, Begoña

    International journal of molecular sciences

    2024  Volume 25, Issue 3

    Abstract: TRPV4 channels, which respond to mechanical activation by permeating ... ...

    Abstract TRPV4 channels, which respond to mechanical activation by permeating Ca
    MeSH term(s) Animals ; Mice ; Calcineurin/metabolism ; Cells, Cultured ; Fibrosis ; Heart Failure/metabolism ; Isoproterenol ; Mice, Transgenic ; Myocytes, Cardiac/metabolism ; NFATC Transcription Factors/genetics ; NFATC Transcription Factors/metabolism ; TRPC6 Cation Channel/genetics ; TRPC6 Cation Channel/metabolism ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism ; Ventricular Remodeling/genetics
    Chemical Substances Calcineurin (EC 3.1.3.16) ; Isoproterenol (L628TT009W) ; NFATC Transcription Factors ; TRPC6 Cation Channel ; TRPV Cation Channels
    Language English
    Publishing date 2024-01-26
    Publishing country Switzerland
    Document type 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/ijms25031541
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  6. Article: Triggering of cardiac preconditioning through Na+/K+-ATPase.

    Inserte, Javier

    Cardiovascular research

    2007  Volume 73, Issue 3, Page(s) 446–447

    MeSH term(s) Enzyme Activation ; Humans ; Ischemic Preconditioning, Myocardial/methods ; Myocardial Ischemia/enzymology ; Myocardial Ischemia/prevention & control ; Myocardium/enzymology ; Ouabain/therapeutic use ; Potassium Channels/metabolism ; Signal Transduction/physiology ; Sodium Channels/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism
    Chemical Substances Potassium Channels ; Sodium Channels ; Ouabain (5ACL011P69) ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
    Language English
    Publishing date 2007-02-01
    Publishing country England
    Document type Comment ; Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1016/j.cardiores.2006.12.008
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    In stock of ZB MED Cologne/Königswinter

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  7. Article ; Online: The cGMP/PKG pathway as a common mediator of cardioprotection: translatability and mechanism.

    Inserte, Javier / Garcia-Dorado, David

    British journal of pharmacology

    2015  Volume 172, Issue 8, Page(s) 1996–2009

    Abstract: Cardiomyocyte cell death occurring during myocardial reperfusion (reperfusion injury) contributes to final infarct size after transient coronary occlusion. Different interrelated mechanisms of reperfusion injury have been identified, including ... ...

    Abstract Cardiomyocyte cell death occurring during myocardial reperfusion (reperfusion injury) contributes to final infarct size after transient coronary occlusion. Different interrelated mechanisms of reperfusion injury have been identified, including alterations in cytosolic Ca(2+) handling, sarcoplasmic reticulum-mediated Ca(2+) oscillations and hypercontracture, proteolysis secondary to calpain activation and mitochondrial permeability transition. All these mechanisms occur during the initial minutes of reperfusion and are inhibited by intracellular acidosis. The cGMP/PKG pathway modulates the rate of recovery of intracellular pH, but has also direct effect on Ca(2+) oscillations and mitochondrial permeability transition. The cGMP/PKG pathway is depressed in cardiomyocytes by ischaemia/reperfusion and preserved by ischaemic postconditioning, which importantly contributes to postconditioning protection. The present article reviews the mechanisms and consequences of the effect of ischaemic postconditioning on the cGMP/PKG pathway, the different pharmacological strategies aimed to stimulate it during myocardial reperfusion and the evidence, limitations and promise of translation of these strategies to the clinical practice. Overall, the preclinical and clinical evidence suggests that modulation of the cGMP/PKG pathway may be a therapeutic target in the context of myocardial infarction.
    MeSH term(s) Animals ; Cardiotonic Agents/pharmacology ; Cardiotonic Agents/therapeutic use ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinases/metabolism ; Humans ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/prevention & control ; Signal Transduction/drug effects
    Chemical Substances Cardiotonic Agents ; Cyclic GMP-Dependent Protein Kinases (EC 2.7.11.12) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2015-03-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.12959
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    Uf I Zs.146: Show issues Location:
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  8. Article ; Online: Citric Acid Cycle Metabolites Predict Infarct Size in

    Consegal, Marta / Núñez, Norberto / Barba, Ignasi / Benito, Begoña / Ruiz-Meana, Marisol / Inserte, Javier / Ferreira-González, Ignacio / Rodríguez-Sinovas, Antonio

    International journal of molecular sciences

    2021  Volume 22, Issue 8

    Abstract: Succinate dehydrogenase (SDH) inhibition with malonate during reperfusion reduced myocardial infarction in animals, whereas its endogenous substrate, succinate, is detected in plasma from STEMI patients. We investigated whether protection by SDH ... ...

    Abstract Succinate dehydrogenase (SDH) inhibition with malonate during reperfusion reduced myocardial infarction in animals, whereas its endogenous substrate, succinate, is detected in plasma from STEMI patients. We investigated whether protection by SDH inhibition is additive to that of remote ischemic perconditioning (RIC) in
    MeSH term(s) Animals ; Biomarkers/blood ; Biomarkers/metabolism ; Citric Acid Cycle ; Coronary Occlusion/metabolism ; Coronary Occlusion/pathology ; Coronary Occlusion/therapy ; Dicarboxylic Acids/blood ; Dicarboxylic Acids/metabolism ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Heart/drug effects ; Ischemic Preconditioning/methods ; Myocardial Infarction/metabolism ; Myocardial Infarction/pathology ; Myocardial Infarction/therapy ; Myocardium/metabolism ; Succinate Dehydrogenase/antagonists & inhibitors ; Swine
    Chemical Substances Biomarkers ; Dicarboxylic Acids ; Enzyme Inhibitors ; Succinate Dehydrogenase (EC 1.3.99.1)
    Language English
    Publishing date 2021-04-16
    Publishing country Switzerland
    Document type 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/ijms22084151
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  9. Article ; Online: Degradation of GRK2 and AKT is an early and detrimental event in myocardial ischemia/reperfusion.

    Penela, Petronila / Inserte, Javier / Ramos, Paula / Rodriguez-Sinovas, Antonio / Garcia-Dorado, David / Mayor, Federico

    EBioMedicine

    2019  Volume 48, Page(s) 605–618

    Abstract: Background: Identification of signaling pathways altered at early stages after cardiac ischemia/reperfusion (I/R) is crucial to develop timely therapies aimed at reducing I/R injury. The expression of G protein-coupled receptor kinase 2 (GRK2), a key ... ...

    Abstract Background: Identification of signaling pathways altered at early stages after cardiac ischemia/reperfusion (I/R) is crucial to develop timely therapies aimed at reducing I/R injury. The expression of G protein-coupled receptor kinase 2 (GRK2), a key signaling hub, is up-regulated in the long-term in patients and in experimental models of heart failure. However, whether GRK2 levels change at early time points following myocardial I/R and its functional impact during this period remain to be established.
    Methods: We have investigated the temporal changes of GRK2 expression and their potential relationships with the cardioprotective AKT pathway in isolated rat hearts and porcine preclinical models of I/R.
    Findings: Contrary to the maladaptive up-regulation of GRK2 reported at later times after myocardial infarction, successive GRK2 phosphorylation at specific sites during ischemia and early reperfusion elicits GRK2 degradation by the proteasome and calpains, respectively, thus keeping GRK2 levels low during early I/R in rat hearts. Concurrently, I/R promotes decay of the prolyl-isomerase Pin1, a positive regulator of AKT stability, and a marked loss of total AKT protein, resulting in an overall decreased activity of this pro-survival pathway. A similar pattern of concomitant down-modulation of GRK2/AKT/Pin1 protein levels in early I/R was observed in pig hearts. Calpain and proteasome inhibition prevents GRK2/Pin1/AKT degradation, restores bulk AKT pathway activity and attenuates myocardial I/R injury in isolated rat hearts.
    Interpretation: Preventing transient degradation of GRK2 and AKT during early I/R might improve the potential of endogenous cardioprotection mechanisms and of conditioning strategies.
    MeSH term(s) Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Biomarkers ; Cells, Cultured ; Disease Models, Animal ; G-Protein-Coupled Receptor Kinase 2/metabolism ; Male ; Models, Biological ; Myocardial Ischemia/etiology ; Myocardial Ischemia/metabolism ; Myocardial Ischemia/pathology ; Myocardial Reperfusion Injury/genetics ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/pathology ; Oxidation-Reduction ; Phosphorylation ; Proteasome Endopeptidase Complex/metabolism ; Proteolysis ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Swine
    Chemical Substances Adaptor Proteins, Signal Transducing ; Biomarkers ; PDZD2 protein, rat ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Grk2 protein, rat (EC 2.7.11.15) ; G-Protein-Coupled Receptor Kinase 2 (EC 2.7.11.16) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2019-10-05
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2851331-9
    ISSN 2352-3964
    ISSN (online) 2352-3964
    DOI 10.1016/j.ebiom.2019.09.019
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 7090: Show issues Location:
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  10. Article ; Online: Connexin 43 Deficiency Is Associated with Reduced Myocardial Scar Size and Attenuated TGFβ1 Signaling after Transient Coronary Occlusion in Conditional Knock-Out Mice.

    Valls-Lacalle, Laura / Consegal, Marta / Ruiz-Meana, Marisol / Benito, Begoña / Inserte, Javier / Barba, Ignasi / Ferreira-González, Ignacio / Rodríguez-Sinovas, Antonio

    Biomolecules

    2020  Volume 10, Issue 4

    Abstract: Previous studies demonstrated a reduction in myocardial scar size in heterozygous ... ...

    Abstract Previous studies demonstrated a reduction in myocardial scar size in heterozygous Cx43
    MeSH term(s) Animals ; Biomarkers/metabolism ; Cicatrix/pathology ; Connective Tissue Growth Factor/metabolism ; Connexin 43/deficiency ; Connexin 43/metabolism ; Coronary Occlusion/diagnostic imaging ; Coronary Occlusion/metabolism ; Coronary Occlusion/pathology ; Coronary Occlusion/physiopathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Myocardium/pathology ; NF-kappa B/metabolism ; Phosphorylation ; Signal Transduction ; Smad Proteins/metabolism ; Transforming Growth Factor beta1/metabolism ; Ventricular Remodeling
    Chemical Substances Biomarkers ; Connexin 43 ; NF-kappa B ; Smad Proteins ; Transforming Growth Factor beta1 ; Connective Tissue Growth Factor (139568-91-5)
    Language English
    Publishing date 2020-04-23
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom10040651
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