| dc.creator | Mattiazzi, Alicia Ramona | |
| dc.creator | Vittone, Leticia | |
| dc.creator | Mundiña-Weilenmann, Cecilia | |
| dc.date | 2007 | |
| dc.date | 2019-10-11T18:11:20Z | |
| dc.identifier | http://sedici.unlp.edu.ar/handle/10915/83199 | |
| dc.identifier | issn:0008-6363 | |
| dc.description | Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery. | |
| dc.description | Facultad de Ciencias Médicas | |
| dc.format | application/pdf | |
| dc.format | 648-656 | |
| dc.language | en | |
| dc.rights | http://creativecommons.org/licenses/by-nc-sa/4.0/ | |
| dc.rights | Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) | |
| dc.subject | Ciencias Médicas | |
| dc.subject | Acidosis | |
| dc.subject | CaMKII | |
| dc.subject | Protein phosphorylation | |
| dc.subject | SR function | |
| dc.title | Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis | |
| dc.type | Articulo | |
| dc.type | Revision | |
