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Cardiac calcium handling on trial: editorial
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| Veröffentlicht in: | Circulation research 114(2014), 1, Seite 12-14 |
|---|---|
| Personen und Körperschaften: | , , , |
| Titel: | Cardiac calcium handling on trial: editorial/ Sven T. Pleger, Philip Raake, Hugo A. Katus, Patrick Most |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
January 2, 2014
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| Gesamtaufnahme: |
: Circulation research, 114(2014), 1, Seite 12-14
, volume:114 |
| Schlagwörter: | |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 520 | |a Targeting abnormal calcium (Ca)2+ handling in ventricular cardiomyocytes emerged as a new paradigm for human heart failure (HF) therapy.1 Cardiomyocytes come with an extensive Ca2+ signaling toolkit consisting of various Ca2+ transporters, Ca2+ channels, Ca2+ buffer, and sensor proteins. Organized into self-contained signaling modules in which Ca2+ signaling functions within highly localized environments, the cardiac Ca2+ signalosome delivers dynamic signals with different spatial and temporal properties that relay compartmentalized Ca2+ oscillations into specific cellular functions.2 As a result, Ca2+ governs not only the cardiomyocyte contractile cycle, but also concurrently control transcription and muscle growth, electric excitability, cell survival, and energy metabolism.3 Article, see p 101. Key components of the cardiac Ca2+ signalosome remodel as a molecular hallmark in HF: loss of sarco(endo)plasmic reticulum ATPase 2a (SERCA2a) expression surfaced as 1 critical abnormality in experimental HF and human failing myocardium. The defect alone is sufficient to disable various Ca2+-dependent homeostatic mechanisms that drive further deterioration of cardiac function and structure after a primary insult, such as myocardial infarction.1 Translational studies, particularly in human-relevant large animal models, have successfully used recombinant adeno-associated viral (rAAV) vectors for cardiac- targeted delivery of therapeutically formulated synthetic SERCA2a DNA that resulted in safe and long-term restoration of cardiac function and reversal of structural, electric, and metabolic remodeling in experimental HF.4 Hence, targeting defective components of the cardiomyocyte Ca2+ signalosome in HF might bear therapeutic benefits beyond sole improvement of cardiac contractile performance (Figure). Figure. Calcium (Ca)2+ regulation of cardiomyocyte function is not limited to contractile performance but extends to control over nuclear transcription, electric activity, cell survival, and energy metabolism . … | ||
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| contents | Targeting abnormal calcium (Ca)2+ handling in ventricular cardiomyocytes emerged as a new paradigm for human heart failure (HF) therapy.1 Cardiomyocytes come with an extensive Ca2+ signaling toolkit consisting of various Ca2+ transporters, Ca2+ channels, Ca2+ buffer, and sensor proteins. Organized into self-contained signaling modules in which Ca2+ signaling functions within highly localized environments, the cardiac Ca2+ signalosome delivers dynamic signals with different spatial and temporal properties that relay compartmentalized Ca2+ oscillations into specific cellular functions.2 As a result, Ca2+ governs not only the cardiomyocyte contractile cycle, but also concurrently control transcription and muscle growth, electric excitability, cell survival, and energy metabolism.3 Article, see p 101. Key components of the cardiac Ca2+ signalosome remodel as a molecular hallmark in HF: loss of sarco(endo)plasmic reticulum ATPase 2a (SERCA2a) expression surfaced as 1 critical abnormality in experimental HF and human failing myocardium. The defect alone is sufficient to disable various Ca2+-dependent homeostatic mechanisms that drive further deterioration of cardiac function and structure after a primary insult, such as myocardial infarction.1 Translational studies, particularly in human-relevant large animal models, have successfully used recombinant adeno-associated viral (rAAV) vectors for cardiac- targeted delivery of therapeutically formulated synthetic SERCA2a DNA that resulted in safe and long-term restoration of cardiac function and reversal of structural, electric, and metabolic remodeling in experimental HF.4 Hence, targeting defective components of the cardiomyocyte Ca2+ signalosome in HF might bear therapeutic benefits beyond sole improvement of cardiac contractile performance (Figure). Figure. Calcium (Ca)2+ regulation of cardiomyocyte function is not limited to contractile performance but extends to control over nuclear transcription, electric activity, cell survival, and energy metabolism . … |
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| spelling | Pleger, Sven Torsten 1973- VerfasserIn (DE-588)129962473 (DE-627)484985221 (DE-576)297924001 aut, Cardiac calcium handling on trial editorial Sven T. Pleger, Philip Raake, Hugo A. Katus, Patrick Most, January 2, 2014, 3, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Gesehen am 23.12.2016, Targeting abnormal calcium (Ca)2+ handling in ventricular cardiomyocytes emerged as a new paradigm for human heart failure (HF) therapy.1 Cardiomyocytes come with an extensive Ca2+ signaling toolkit consisting of various Ca2+ transporters, Ca2+ channels, Ca2+ buffer, and sensor proteins. Organized into self-contained signaling modules in which Ca2+ signaling functions within highly localized environments, the cardiac Ca2+ signalosome delivers dynamic signals with different spatial and temporal properties that relay compartmentalized Ca2+ oscillations into specific cellular functions.2 As a result, Ca2+ governs not only the cardiomyocyte contractile cycle, but also concurrently control transcription and muscle growth, electric excitability, cell survival, and energy metabolism.3 Article, see p 101. Key components of the cardiac Ca2+ signalosome remodel as a molecular hallmark in HF: loss of sarco(endo)plasmic reticulum ATPase 2a (SERCA2a) expression surfaced as 1 critical abnormality in experimental HF and human failing myocardium. The defect alone is sufficient to disable various Ca2+-dependent homeostatic mechanisms that drive further deterioration of cardiac function and structure after a primary insult, such as myocardial infarction.1 Translational studies, particularly in human-relevant large animal models, have successfully used recombinant adeno-associated viral (rAAV) vectors for cardiac- targeted delivery of therapeutically formulated synthetic SERCA2a DNA that resulted in safe and long-term restoration of cardiac function and reversal of structural, electric, and metabolic remodeling in experimental HF.4 Hence, targeting defective components of the cardiomyocyte Ca2+ signalosome in HF might bear therapeutic benefits beyond sole improvement of cardiac contractile performance (Figure). Figure. Calcium (Ca)2+ regulation of cardiomyocyte function is not limited to contractile performance but extends to control over nuclear transcription, electric activity, cell survival, and energy metabolism . …, calcium signaling, Editorials, genetic therapy, heart failure, Raake, Philip 1975- VerfasserIn (DE-588)129151246 (DE-627)390021725 (DE-576)297510568 aut, Katus, Hugo 1951- VerfasserIn (DE-588)108916618 (DE-627)577155040 (DE-576)289625076 aut, Most, Patrick 1969- VerfasserIn (DE-588)124606431 (DE-627)363440267 (DE-576)29440919X aut, Enthalten in Circulation research New York, NY : Assoc., 1953 114(2014), 1, Seite 12-14 Online-Ressource (DE-627)266880126 (DE-600)1467838-X (DE-576)075145766 1524-4571 nnns, volume:114 year:2014 number:1 pages:12-14 extent:3, http://dx.doi.org/10.1161/CIRCRESAHA.113.302748 Verlag Resolving-System kostenfrei Volltext, http://circres.ahajournals.org/content/114/1/12 Verlag Volltext, http://dx.doi.org/10.1161/CIRCRESAHA.113.302748 LFER, LFER 2017-01-16T00:00:00Z |
| spellingShingle | Pleger, Sven Torsten, Raake, Philip, Katus, Hugo, Most, Patrick, Cardiac calcium handling on trial: editorial, Targeting abnormal calcium (Ca)2+ handling in ventricular cardiomyocytes emerged as a new paradigm for human heart failure (HF) therapy.1 Cardiomyocytes come with an extensive Ca2+ signaling toolkit consisting of various Ca2+ transporters, Ca2+ channels, Ca2+ buffer, and sensor proteins. Organized into self-contained signaling modules in which Ca2+ signaling functions within highly localized environments, the cardiac Ca2+ signalosome delivers dynamic signals with different spatial and temporal properties that relay compartmentalized Ca2+ oscillations into specific cellular functions.2 As a result, Ca2+ governs not only the cardiomyocyte contractile cycle, but also concurrently control transcription and muscle growth, electric excitability, cell survival, and energy metabolism.3 Article, see p 101. Key components of the cardiac Ca2+ signalosome remodel as a molecular hallmark in HF: loss of sarco(endo)plasmic reticulum ATPase 2a (SERCA2a) expression surfaced as 1 critical abnormality in experimental HF and human failing myocardium. The defect alone is sufficient to disable various Ca2+-dependent homeostatic mechanisms that drive further deterioration of cardiac function and structure after a primary insult, such as myocardial infarction.1 Translational studies, particularly in human-relevant large animal models, have successfully used recombinant adeno-associated viral (rAAV) vectors for cardiac- targeted delivery of therapeutically formulated synthetic SERCA2a DNA that resulted in safe and long-term restoration of cardiac function and reversal of structural, electric, and metabolic remodeling in experimental HF.4 Hence, targeting defective components of the cardiomyocyte Ca2+ signalosome in HF might bear therapeutic benefits beyond sole improvement of cardiac contractile performance (Figure). Figure. Calcium (Ca)2+ regulation of cardiomyocyte function is not limited to contractile performance but extends to control over nuclear transcription, electric activity, cell survival, and energy metabolism . …, calcium signaling, Editorials, genetic therapy, heart failure |
| swb_id_str | 481262083 |
| title | Cardiac calcium handling on trial: editorial |
| title_auth | Cardiac calcium handling on trial editorial |
| title_full | Cardiac calcium handling on trial editorial Sven T. Pleger, Philip Raake, Hugo A. Katus, Patrick Most |
| title_fullStr | Cardiac calcium handling on trial editorial Sven T. Pleger, Philip Raake, Hugo A. Katus, Patrick Most |
| title_full_unstemmed | Cardiac calcium handling on trial editorial Sven T. Pleger, Philip Raake, Hugo A. Katus, Patrick Most |
| title_in_hierarchy | Cardiac calcium handling on trial: editorial / Sven T. Pleger, Philip Raake, Hugo A. Katus, Patrick Most, |
| title_short | Cardiac calcium handling on trial |
| title_sort | cardiac calcium handling on trial editorial |
| title_sub | editorial |
| topic | calcium signaling, Editorials, genetic therapy, heart failure |
| topic_facet | calcium signaling, Editorials, genetic therapy, heart failure |
| url | http://dx.doi.org/10.1161/CIRCRESAHA.113.302748, http://circres.ahajournals.org/content/114/1/12 |