Abstract
Synchronized SR calcium (Ca) release is critical to normal cardiac myocyte excitation-contraction coupling, and ideally this release shuts off completely between heartbeats. However, other SR Ca release events are referred to collectively as SR Ca leak (which includes Ca sparks and waves as well as smaller events not detectable as Ca sparks). Much, but not all, of the SR Ca leak occurs via ryanodine receptors and can be exacerbated in pathological states such as heart failure. The extent of SR Ca leak is important because it can (a) reduce SR Ca available for release, causing systolic dysfunction; (b) elevate diastolic Cai, contributing to diastolic dysfunction; (c) cause triggered arrhythmias; and (d) be energetically costly because of extra ATP used to repump Ca. This review addresses quantitative aspects and manifestations of SR Ca leak and its measurement, and how leak is modulated by Ca, associated proteins, and posttranslational modifications in health and disease. ©
| Original language | English (US) |
|---|---|
| Pages (from-to) | 107-127 |
| Number of pages | 21 |
| Journal | Annual Review of Physiology |
| Volume | 76 |
| DOIs | |
| State | Published - Feb 2014 |
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Keywords
- Calcium
- Cardiac muscle
- Ryanodine receptor
- Sarcoplasmic reticulum
ASJC Scopus subject areas
- Physiology
Cite this
Cardiac sarcoplasmic reticulum calcium leak : Basis and roles in cardiac dysfunction. / Bers, Donald M.
In: Annual Review of Physiology, Vol. 76, 02.2014, p. 107-127.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cardiac sarcoplasmic reticulum calcium leak
T2 - Basis and roles in cardiac dysfunction
AU - Bers, Donald M
PY - 2014/2
Y1 - 2014/2
N2 - Synchronized SR calcium (Ca) release is critical to normal cardiac myocyte excitation-contraction coupling, and ideally this release shuts off completely between heartbeats. However, other SR Ca release events are referred to collectively as SR Ca leak (which includes Ca sparks and waves as well as smaller events not detectable as Ca sparks). Much, but not all, of the SR Ca leak occurs via ryanodine receptors and can be exacerbated in pathological states such as heart failure. The extent of SR Ca leak is important because it can (a) reduce SR Ca available for release, causing systolic dysfunction; (b) elevate diastolic Cai, contributing to diastolic dysfunction; (c) cause triggered arrhythmias; and (d) be energetically costly because of extra ATP used to repump Ca. This review addresses quantitative aspects and manifestations of SR Ca leak and its measurement, and how leak is modulated by Ca, associated proteins, and posttranslational modifications in health and disease. ©
AB - Synchronized SR calcium (Ca) release is critical to normal cardiac myocyte excitation-contraction coupling, and ideally this release shuts off completely between heartbeats. However, other SR Ca release events are referred to collectively as SR Ca leak (which includes Ca sparks and waves as well as smaller events not detectable as Ca sparks). Much, but not all, of the SR Ca leak occurs via ryanodine receptors and can be exacerbated in pathological states such as heart failure. The extent of SR Ca leak is important because it can (a) reduce SR Ca available for release, causing systolic dysfunction; (b) elevate diastolic Cai, contributing to diastolic dysfunction; (c) cause triggered arrhythmias; and (d) be energetically costly because of extra ATP used to repump Ca. This review addresses quantitative aspects and manifestations of SR Ca leak and its measurement, and how leak is modulated by Ca, associated proteins, and posttranslational modifications in health and disease. ©
KW - Calcium
KW - Cardiac muscle
KW - Ryanodine receptor
KW - Sarcoplasmic reticulum
UR - http://www.scopus.com/inward/record.url?scp=84894146350&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84894146350&partnerID=8YFLogxK
U2 - 10.1146/annurev-physiol-020911-153308
DO - 10.1146/annurev-physiol-020911-153308
M3 - Article
VL - 76
SP - 107
EP - 127
JO - Annual Review of Physiology
JF - Annual Review of Physiology
SN - 0066-4278
ER -