Abstract |
Ischemia-reperfusion injury (IRI) has been recognized as a serious problem for therapy of cardiovascular diseases. Calcium regulation appears to be an important issue in the study of IRI. This article reviews calcium regulation in myocardial and vascular IRI, including the calcium overload and calcium sensitivity in IRI. This review is focused on the key players in Ca(2+) handling in IRI, including membrane damage resulting in increase in Ca(2+) influx, reverse-mode of Na(+)-Ca(2+) exchangers leading to increased Ca(2+) entry, the decreased activity of sarcoplasmic reticulum (SR) Ca(2+)- ATPase causing SR Ca(2+) uptake dysfunction, and increased activity of Rho kinase. These key players in Ca(2+) homeostasis will provide promising strategies and potential targets for therapy of cardiovascular IRI.
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Authors | Xi He, Xue-Yuan Bi, Hao Wang, Xiao-Jiang Yu, Wei-Jin Zang |
Journal | Sheng li xue bao : [Acta physiologica Sinica]
(Sheng Li Xue Bao)
Vol. 64
Issue 3
Pg. 321-6
(Jun 25 2012)
ISSN: 0371-0874 [Print] China |
PMID | 22717637
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Sodium-Calcium Exchanger
- Sarcoplasmic Reticulum Calcium-Transporting ATPases
- Calcium
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Topics |
- Animals
- Calcium
(metabolism)
- Heart
(physiopathology)
- Homeostasis
- Humans
- Myocardial Reperfusion Injury
(metabolism)
- Myocardium
- Sarcoplasmic Reticulum
(metabolism)
- Sarcoplasmic Reticulum Calcium-Transporting ATPases
(metabolism)
- Sodium-Calcium Exchanger
(metabolism)
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