Structural and functional alterations in the Ca$^2+$ regulatory
proteins present in the sarcoplasmic reticulum have recently been
shown to be strongly involved in the pathogenesis of heart failure.
Chronic activation of the sympathetic nervous system or of the renin-angiotensin
system induces abnormalities in both the function and structure of
these proteins. We review here the considerable body of evidence
that has accumulated to support the notion that such abnormalities
contribute to a defectiveness of contractile performance and hence
to the progression of heart failure.
%0 Journal Article
%1 Yano_2005_556
%A Yano, Masafumi
%A Ikeda, Yasuhiro
%A Matsuzaki, Masunori
%D 2005
%J J. Clin. Invest.
%K 15765137 Animals, Calcium Calcium, Calcium-Binding Cardiac Cardiac, Cardiomyopathy, Channel, Contraction, Gov't, Humans, Hypertrophic, Low, Muscle Myocardial Myocytes, Non-U.S. Output, Proteins, Receptor Release Research Reticulum, Ryanodine Sarcoplasmic Signaling, Support,
%N 3
%P 556--564
%R 10.1172/JCI200524159
%T Altered intracellular Ca$^2+$ handling in heart failure.
%U http://dx.doi.org/10.1172/JCI200524159
%V 115
%X Structural and functional alterations in the Ca$^2+$ regulatory
proteins present in the sarcoplasmic reticulum have recently been
shown to be strongly involved in the pathogenesis of heart failure.
Chronic activation of the sympathetic nervous system or of the renin-angiotensin
system induces abnormalities in both the function and structure of
these proteins. We review here the considerable body of evidence
that has accumulated to support the notion that such abnormalities
contribute to a defectiveness of contractile performance and hence
to the progression of heart failure.
@article{Yano_2005_556,
abstract = {Structural and functional alterations in the {C}a$^{2+}$ regulatory
proteins present in the sarcoplasmic reticulum have recently been
shown to be strongly involved in the pathogenesis of heart failure.
Chronic activation of the sympathetic nervous system or of the renin-angiotensin
system induces abnormalities in both the function and structure of
these proteins. We review here the considerable body of evidence
that has accumulated to support the notion that such abnormalities
contribute to a defectiveness of contractile performance and hence
to the progression of heart failure.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Yano, Masafumi and Ikeda, Yasuhiro and Matsuzaki, Masunori},
biburl = {https://www.bibsonomy.org/bibtex/234eca806a093034eb5cd17d932ce139b/hake},
description = {The whole bibliography file I use.},
doi = {10.1172/JCI200524159},
file = {Yano_2005_556.pdf:Yano_2005_556.pdf:PDF},
interhash = {2e361eee2dedea7cd62c1e0afd0b43d9},
intrahash = {34eca806a093034eb5cd17d932ce139b},
journal = {J. Clin. Invest.},
keywords = {15765137 Animals, Calcium Calcium, Calcium-Binding Cardiac Cardiac, Cardiomyopathy, Channel, Contraction, Gov't, Humans, Hypertrophic, Low, Muscle Myocardial Myocytes, Non-U.S. Output, Proteins, Receptor Release Research Reticulum, Ryanodine Sarcoplasmic Signaling, Support,},
month = Mar,
number = 3,
pages = {556--564},
pmid = {15765137},
timestamp = {2009-06-03T11:21:38.000+0200},
title = {Altered intracellular {C}a$^{2+}$ handling in heart failure.},
url = {http://dx.doi.org/10.1172/JCI200524159},
volume = 115,
year = 2005
}