Signal Transduction and Cardiac Hypertrophy:
Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for th...
Gespeichert in:
| Weitere beteiligte Personen: | , , , |
|---|---|
| Format: | Elektronisch E-Book |
| Sprache: | Englisch |
| Veröffentlicht: |
Boston, MA
Springer US
2003
|
| Schriftenreihe: | Progress in Experimental Cardiology
7 |
| Schlagwörter: | |
| Links: | https://doi.org/10.1007/978-1-4615-0347-7 https://doi.org/10.1007/978-1-4615-0347-7 |
| Zusammenfassung: | Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor mation is beginning to provide tangible targets towards manipulating cardiac func tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben eficial response under many conditions, it can be highly deleterious and inappropri ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben eficial |
| Umfang: | 1 Online-Ressource (XVII, 508 p) |
| ISBN: | 9781461503477 |
| DOI: | 10.1007/978-1-4615-0347-7 |
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| 520 | |a Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor mation is beginning to provide tangible targets towards manipulating cardiac func tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben eficial response under many conditions, it can be highly deleterious and inappropri ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben eficial | ||
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| discipline | Medizin |
| doi_str_mv | 10.1007/978-1-4615-0347-7 |
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| id | DE-604.BV046144205 |
| illustrated | Not Illustrated |
| indexdate | 2024-12-20T18:44:16Z |
| institution | BVB |
| isbn | 9781461503477 |
| language | English |
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| series2 | Progress in Experimental Cardiology |
| spelling | Signal Transduction and Cardiac Hypertrophy edited by Naranjan S. Dhalla, Larry V. Hryshko, Elissavet Kardami, Pawan K. Singal Boston, MA Springer US 2003 1 Online-Ressource (XVII, 508 p) txt rdacontent c rdamedia cr rdacarrier Progress in Experimental Cardiology 7 Cellular signaling in cardiac muscle refers to the myriad of stimuli and responses that direct and control the physiological operation of this organ. Our understand ing of these complex signaling cascades has increased dramatically over the past few decades with the advent of molecular tools for their dissection. Moreover, this infor mation is beginning to provide tangible targets towards manipulating cardiac func tion in the setting of cardiovascular disease. The mechanisms and factors that regulate cardiac cell growth are of particular interest as both adaptive and maladaptive responses can occur during cardiac hypertrophy. Cardiac hypertrophy describes the increase in individual cardiac myocyte size that is accomplished through the series and/or parallel addition of sarcomeres. The ability of cardiac muscle to increase in size through hyperplasia becomes highly restricted or negligible shortly after birth. Consequently, the increase in heart size associated with development and growth of an individual occurs through hypertrophy. In response to a chronic increase in workload, cardiac muscle cells can dramatically increase in size to face their increasing contractile demands. While this plasticity is clearly a ben eficial response under many conditions, it can be highly deleterious and inappropri ate under others. For example, cardiac hypertrophy associated with endurance exercise clearly enhances athletic performance. In contrast, the hypertrophy associated with chronic hypertension, stenotic or regurgitant heart valves, or following a myocardial infarction often continues far beyond the period where this adaptive response is ben eficial Cardiology Dhalla, Naranjan S. edt Hryshko, Larry V. edt Kardami, Elissavet edt Singal, Pawan K. edt Erscheint auch als Druck-Ausgabe 9781402072185 Erscheint auch als Druck-Ausgabe 9781461350323 Erscheint auch als Druck-Ausgabe 9781461503484 https://doi.org/10.1007/978-1-4615-0347-7 Verlag URL des Erstveröffentlichers Volltext |
| spellingShingle | Signal Transduction and Cardiac Hypertrophy Cardiology |
| title | Signal Transduction and Cardiac Hypertrophy |
| title_auth | Signal Transduction and Cardiac Hypertrophy |
| title_exact_search | Signal Transduction and Cardiac Hypertrophy |
| title_full | Signal Transduction and Cardiac Hypertrophy edited by Naranjan S. Dhalla, Larry V. Hryshko, Elissavet Kardami, Pawan K. Singal |
| title_fullStr | Signal Transduction and Cardiac Hypertrophy edited by Naranjan S. Dhalla, Larry V. Hryshko, Elissavet Kardami, Pawan K. Singal |
| title_full_unstemmed | Signal Transduction and Cardiac Hypertrophy edited by Naranjan S. Dhalla, Larry V. Hryshko, Elissavet Kardami, Pawan K. Singal |
| title_short | Signal Transduction and Cardiac Hypertrophy |
| title_sort | signal transduction and cardiac hypertrophy |
| topic | Cardiology |
| topic_facet | Cardiology |
| url | https://doi.org/10.1007/978-1-4615-0347-7 |
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