Literature DB >> 35199536

Structure-function relationships and modifications of cardiac sarcoplasmic reticulum Ca2+-transport.

M Nusier1, A K Shah, N S Dhalla.   

Abstract

Sarcoplasmic reticulum (SR) is a specialized tubular network, which not only maintains the intracellular concentration of Ca2+ at a low level but is also known to release and accumulate Ca2+ for the occurrence of cardiac contraction and relaxation, respectively. This subcellular organelle is composed of several phospholipids and different Ca2+-cycling, Ca2+-binding and regulatory proteins, which work in a coordinated manner to determine its function in cardiomyocytes. Some of the major proteins in the cardiac SR membrane include Ca2+-pump ATPase (SERCA2), Ca2+-release protein (ryanodine receptor), calsequestrin (Ca2+-binding protein) and phospholamban (regulatory protein). The phosphorylation of SR Ca2+-cycling proteins by protein kinase A or Ca2+-calmodulin kinase (directly or indirectly) has been demonstrated to augment SR Ca2+-release and Ca2+-uptake activities and promote cardiac contraction and relaxation functions. The activation of phospholipases and proteases as well as changes in different gene expressions under different pathological conditions have been shown to alter the SR composition and produce Ca2+-handling abnormalities in cardiomyocytes for the development of cardiac dysfunction. The post-translational modifications of SR Ca2+ cycling proteins by processes such as oxidation, nitrosylation, glycosylation, lipidation, acetylation, sumoylation, and O GlcNacylation have also been reported to affect the SR Ca2+ release and uptake activities as well as cardiac contractile activity. The SR function in the heart is also influenced in association with changes in cardiac performance by several hormones including thyroid hormones and adiponectin as well as by exercise-training. On the basis of such observations, it is suggested that both Ca2+-cycling and regulatory proteins in the SR membranes are intimately involved in determining the status of cardiac function and are thus excellent targets for drug development for the treatment of heart disease.

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Year:  2021        PMID: 35199536      PMCID: PMC9054189          DOI: 10.33549/physiolres.934805

Source DB:  PubMed          Journal:  Physiol Res        ISSN: 0862-8408            Impact factor:   2.139


  276 in total

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2.  Ryanodine Receptor Glycation Favors Mitochondrial Damage in the Senescent Heart.

Authors:  Marisol Ruiz-Meana; Marta Minguet; Diana Bou-Teen; Elisabet Miro-Casas; Celia Castans; Jose Castellano; Elena Bonzon-Kulichenko; Alberto Igual; Rafael Rodriguez-Lecoq; Jesús Vázquez; David Garcia-Dorado
Journal:  Circulation       Date:  2019-02-12       Impact factor: 29.690

3.  Excitation-contraction coupling in heart. V. Contribution of mitochondria and sarcoplasmic reticulum in the regulation of calcium concentration in the heart.

Authors:  N S Dhalla; D B McNamara; P V Sulakhe
Journal:  Cardiology       Date:  1970       Impact factor: 1.869

Review 4.  The SarcoEndoplasmic Reticulum Calcium ATPase.

Authors:  Joseph O Primeau; Gareth P Armanious; M'Lynn E Fisher; Howard S Young
Journal:  Subcell Biochem       Date:  2018

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Journal:  Circ Res       Date:  2017-06-09       Impact factor: 17.367

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Authors:  Xinyu Zhou; Ki Ho Park; Daiju Yamazaki; Pei-Hui Lin; Miyuki Nishi; Zhiwei Ma; Liming Qiu; Takashi Murayama; Xiaoqin Zou; Hiroshi Takeshima; Jingsong Zhou; Jianjie Ma
Journal:  Circ Res       Date:  2019-12-06       Impact factor: 17.367

Review 7.  Ryanodine receptors: structure, expression, molecular details, and function in calcium release.

Authors:  Johanna T Lanner; Dimitra K Georgiou; Aditya D Joshi; Susan L Hamilton
Journal:  Cold Spring Harb Perspect Biol       Date:  2010-10-20       Impact factor: 10.005

8.  Plasma adiponectin levels and risk of myocardial infarction in men.

Authors:  Tobias Pischon; Cynthia J Girman; Gokhan S Hotamisligil; Nader Rifai; Frank B Hu; Eric B Rimm
Journal:  JAMA       Date:  2004-04-14       Impact factor: 56.272

9.  Diabetes and the accompanying hyperglycemia impairs cardiomyocyte calcium cycling through increased nuclear O-GlcNAcylation.

Authors:  Raymond J Clark; Patrick M McDonough; Eric Swanson; Susanne U Trost; Misa Suzuki; Minoru Fukuda; Wolfgang H Dillmann
Journal:  J Biol Chem       Date:  2003-08-26       Impact factor: 5.157

10.  Physical interaction of junctophilin and the CaV1.1 C terminus is crucial for skeletal muscle contraction.

Authors:  Tsutomu Nakada; Toshihide Kashihara; Masatoshi Komatsu; Katsuhiko Kojima; Toshikazu Takeshita; Mitsuhiko Yamada
Journal:  Proc Natl Acad Sci U S A       Date:  2018-04-09       Impact factor: 11.205

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