Abstract
Regulation of Calcium (Ca) cycling by the sarcoplasmic reticulum (SR) underlies the control of cardiac contraction during excitation-contraction (E-C) coupling. Moreover, alterations in E-C coupling occurring in cardiac hypertrophy and heart failure are characterized by abnormal Ca-cycling through the SR network. A large body of evidence points to the central role of: a) SERCA and its regulator phospholamban (PLN) in the modulation of cardiac relaxation; b) calsequestrin in the regulation of SR Ca-load; and c) the ryanodine receptor (RyR) Ca-channel in the control of SR Ca-release. The levels or activity of these key Ca-handling proteins are altered in cardiomyopathies, and these changes have been linked to the deteriorated cardiac function and remodeling. Furthermore, genetic variants in these SR Ca-cycling proteins have been identified, which may predispose to heart failure or fatal arrhythmias. This chapter concentrates on the pivotal role of SR Ca-cycling proteins in health and disease with specific emphasis on their recently reported genetic modifiers.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 523-537 |
| Number of pages | 15 |
| Journal | Sub-Cellular Biochemistry |
| Volume | 45 |
| State | Published - 2007 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
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Calcium and cardiomyopathies. / Kranias, E. G.; Bers, Donald M.
In: Sub-Cellular Biochemistry, Vol. 45, 2007, p. 523-537.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Calcium and cardiomyopathies.
AU - Kranias, E. G.
AU - Bers, Donald M
PY - 2007
Y1 - 2007
N2 - Regulation of Calcium (Ca) cycling by the sarcoplasmic reticulum (SR) underlies the control of cardiac contraction during excitation-contraction (E-C) coupling. Moreover, alterations in E-C coupling occurring in cardiac hypertrophy and heart failure are characterized by abnormal Ca-cycling through the SR network. A large body of evidence points to the central role of: a) SERCA and its regulator phospholamban (PLN) in the modulation of cardiac relaxation; b) calsequestrin in the regulation of SR Ca-load; and c) the ryanodine receptor (RyR) Ca-channel in the control of SR Ca-release. The levels or activity of these key Ca-handling proteins are altered in cardiomyopathies, and these changes have been linked to the deteriorated cardiac function and remodeling. Furthermore, genetic variants in these SR Ca-cycling proteins have been identified, which may predispose to heart failure or fatal arrhythmias. This chapter concentrates on the pivotal role of SR Ca-cycling proteins in health and disease with specific emphasis on their recently reported genetic modifiers.
AB - Regulation of Calcium (Ca) cycling by the sarcoplasmic reticulum (SR) underlies the control of cardiac contraction during excitation-contraction (E-C) coupling. Moreover, alterations in E-C coupling occurring in cardiac hypertrophy and heart failure are characterized by abnormal Ca-cycling through the SR network. A large body of evidence points to the central role of: a) SERCA and its regulator phospholamban (PLN) in the modulation of cardiac relaxation; b) calsequestrin in the regulation of SR Ca-load; and c) the ryanodine receptor (RyR) Ca-channel in the control of SR Ca-release. The levels or activity of these key Ca-handling proteins are altered in cardiomyopathies, and these changes have been linked to the deteriorated cardiac function and remodeling. Furthermore, genetic variants in these SR Ca-cycling proteins have been identified, which may predispose to heart failure or fatal arrhythmias. This chapter concentrates on the pivotal role of SR Ca-cycling proteins in health and disease with specific emphasis on their recently reported genetic modifiers.
UR - http://www.scopus.com/inward/record.url?scp=38849156470&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=38849156470&partnerID=8YFLogxK
M3 - Article
C2 - 18193651
AN - SCOPUS:38849156470
VL - 45
SP - 523
EP - 537
JO - Sub-Cellular Biochemistry
JF - Sub-Cellular Biochemistry
SN - 0306-0225
ER -