Modulation of sarcoplasmic reticulum function: a new strategy in cardioprotection?
This article reviews the experimental evidence suggesting that cytosolic Ca(2+) overload plays a major role in the development of myocardial injury during ischemia-reperfusion and that Ca(2+) release from the sarcoplasmic reticulum (SR) is of crucial importance in the early phase of ischemia. It is suggested that interventions able to deplete the SR Ca(2+) pool and/or to reduce the rate of SR Ca(2+) release should be cardioprotective. This thesis is supported by the review of experimental studies in which modulators of the SR Ca(2+)-ATPase or SR Ca(2+) release channel (ryanodine receptor) have been used. In addition, the role of the SR in ischemic preconditioning and in some instances of toxic myocardial injury (particularly, anthraquinone-induced injury) is discussed.
Zucchi
R
R
Dipartimento di Scienze dell'Uomo e dell'Ambiente, University of Pisa, via Roma 55, 56126 Pisa, Italy. r.zucchi@med.unipd.it
Ronca
F
F
Ronca-Testoni
S
S
D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D006801:Humans; D019194:Ischemic Preconditioning; D017202:Myocardial Ischemia / Q000378:metabolism / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D019837:Ryanodine Receptor Calcium Release Channel / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000502:physiology*
D019837:Ryanodine Receptor Calcium Release Channel; D000252:Calcium-Transporting ATPases; D002118:Calcium