Calcium cycling circuits in cardiac physiology and pathophysiology

K. Haghighi, D. Sanoudou, E. G. Kranias

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Citation (Scopus)

Abstract

Abnormal calcium cycling is a universal characteristic of human and experimental heart failure. This calcium dysregulation has been mainly attributed to the impaired function of the cardiac sarcoplasmic reticulum (SR). Abnormal Ca2+transport by the SR proteins, Ca2+ATPase (SERCA2a) and phospholamban (PLN), has been shown to have a vital role in cardiac pathophysiology and the progression of heart failure. PLN is an endogenous inhibitor of SERCA2a and as such is a primary player in cardiac relaxation by regulating Ca2+uptake. Moreover, recent studies identified other regulatory proteins in the SR Ca2+transport complex, namely inhibitor1 of protein phosphatase 1 (PP1), the small heat shock protein 20 (Hsp20), the histidinerich calcium binding protein (HRC), and the HS1 associated protein X1 (HAX1). We have shown that these new players could influence the PLN/SERCA activity and consequently, SR Ca2 +transport, cardiomyocyte Ca2 +contractility, cardiac remodeling and cell apoptosis. This article concentrates on the crucial role of the SR Ca2+handling proteins in the regulation of cardiac function and survival under physiological and pathophysiological conditions. The role of naturally occurring variants in these Ca+cycling genes, which may serve as prognostic or diagnostic factors as well as modifiers of heart failure development, is also discussed.

Original languageEnglish
Title of host publicationIntroduction to Translational Cardiovascular Research
PublisherSpringer International Publishing
Pages205-215
Number of pages11
ISBN (Print)9783319087986, 9783319087979
DOIs
Publication statusPublished - 1 Jan 2015
Externally publishedYes

Fingerprint

Sarcoplasmic Reticulum
Calcium
Heart Failure
HSP20 Heat-Shock Proteins
Proteins
Small Heat-Shock Proteins
Protein Phosphatase 1
Calcium-Binding Proteins
Calcium-Transporting ATPases
Cardiac Myocytes
Apoptosis
Survival
Genes
phospholamban

Keywords

  • Calcium
  • Contractility
  • Heart Failure
  • Human Variants
  • Sarcoplasmic Reticulum

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Haghighi, K., Sanoudou, D., & Kranias, E. G. (2015). Calcium cycling circuits in cardiac physiology and pathophysiology. In Introduction to Translational Cardiovascular Research (pp. 205-215). Springer International Publishing. https://doi.org/10.1007/9783319087986_12

Calcium cycling circuits in cardiac physiology and pathophysiology. / Haghighi, K.; Sanoudou, D.; Kranias, E. G.

Introduction to Translational Cardiovascular Research. Springer International Publishing, 2015. p. 205-215.

Research output: Chapter in Book/Report/Conference proceedingChapter

Haghighi, K, Sanoudou, D & Kranias, EG 2015, Calcium cycling circuits in cardiac physiology and pathophysiology. in Introduction to Translational Cardiovascular Research. Springer International Publishing, pp. 205-215. https://doi.org/10.1007/9783319087986_12
Haghighi K, Sanoudou D, Kranias EG. Calcium cycling circuits in cardiac physiology and pathophysiology. In Introduction to Translational Cardiovascular Research. Springer International Publishing. 2015. p. 205-215 https://doi.org/10.1007/9783319087986_12
Haghighi, K. ; Sanoudou, D. ; Kranias, E. G. / Calcium cycling circuits in cardiac physiology and pathophysiology. Introduction to Translational Cardiovascular Research. Springer International Publishing, 2015. pp. 205-215
@inbook{7e8ebbaea1b6490d9be99e52c88f45ca,
title = "Calcium cycling circuits in cardiac physiology and pathophysiology",
abstract = "Abnormal calcium cycling is a universal characteristic of human and experimental heart failure. This calcium dysregulation has been mainly attributed to the impaired function of the cardiac sarcoplasmic reticulum (SR). Abnormal Ca2+transport by the SR proteins, Ca2+ATPase (SERCA2a) and phospholamban (PLN), has been shown to have a vital role in cardiac pathophysiology and the progression of heart failure. PLN is an endogenous inhibitor of SERCA2a and as such is a primary player in cardiac relaxation by regulating Ca2+uptake. Moreover, recent studies identified other regulatory proteins in the SR Ca2+transport complex, namely inhibitor1 of protein phosphatase 1 (PP1), the small heat shock protein 20 (Hsp20), the histidinerich calcium binding protein (HRC), and the HS1 associated protein X1 (HAX1). We have shown that these new players could influence the PLN/SERCA activity and consequently, SR Ca2 +transport, cardiomyocyte Ca2 +contractility, cardiac remodeling and cell apoptosis. This article concentrates on the crucial role of the SR Ca2+handling proteins in the regulation of cardiac function and survival under physiological and pathophysiological conditions. The role of naturally occurring variants in these Ca+cycling genes, which may serve as prognostic or diagnostic factors as well as modifiers of heart failure development, is also discussed.",
keywords = "Calcium, Contractility, Heart Failure, Human Variants, Sarcoplasmic Reticulum",
author = "K. Haghighi and D. Sanoudou and Kranias, {E. G.}",
year = "2015",
month = "1",
day = "1",
doi = "10.1007/9783319087986_12",
language = "English",
isbn = "9783319087986",
pages = "205--215",
booktitle = "Introduction to Translational Cardiovascular Research",
publisher = "Springer International Publishing",

}

TY - CHAP

T1 - Calcium cycling circuits in cardiac physiology and pathophysiology

AU - Haghighi, K.

AU - Sanoudou, D.

AU - Kranias, E. G.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - Abnormal calcium cycling is a universal characteristic of human and experimental heart failure. This calcium dysregulation has been mainly attributed to the impaired function of the cardiac sarcoplasmic reticulum (SR). Abnormal Ca2+transport by the SR proteins, Ca2+ATPase (SERCA2a) and phospholamban (PLN), has been shown to have a vital role in cardiac pathophysiology and the progression of heart failure. PLN is an endogenous inhibitor of SERCA2a and as such is a primary player in cardiac relaxation by regulating Ca2+uptake. Moreover, recent studies identified other regulatory proteins in the SR Ca2+transport complex, namely inhibitor1 of protein phosphatase 1 (PP1), the small heat shock protein 20 (Hsp20), the histidinerich calcium binding protein (HRC), and the HS1 associated protein X1 (HAX1). We have shown that these new players could influence the PLN/SERCA activity and consequently, SR Ca2 +transport, cardiomyocyte Ca2 +contractility, cardiac remodeling and cell apoptosis. This article concentrates on the crucial role of the SR Ca2+handling proteins in the regulation of cardiac function and survival under physiological and pathophysiological conditions. The role of naturally occurring variants in these Ca+cycling genes, which may serve as prognostic or diagnostic factors as well as modifiers of heart failure development, is also discussed.

AB - Abnormal calcium cycling is a universal characteristic of human and experimental heart failure. This calcium dysregulation has been mainly attributed to the impaired function of the cardiac sarcoplasmic reticulum (SR). Abnormal Ca2+transport by the SR proteins, Ca2+ATPase (SERCA2a) and phospholamban (PLN), has been shown to have a vital role in cardiac pathophysiology and the progression of heart failure. PLN is an endogenous inhibitor of SERCA2a and as such is a primary player in cardiac relaxation by regulating Ca2+uptake. Moreover, recent studies identified other regulatory proteins in the SR Ca2+transport complex, namely inhibitor1 of protein phosphatase 1 (PP1), the small heat shock protein 20 (Hsp20), the histidinerich calcium binding protein (HRC), and the HS1 associated protein X1 (HAX1). We have shown that these new players could influence the PLN/SERCA activity and consequently, SR Ca2 +transport, cardiomyocyte Ca2 +contractility, cardiac remodeling and cell apoptosis. This article concentrates on the crucial role of the SR Ca2+handling proteins in the regulation of cardiac function and survival under physiological and pathophysiological conditions. The role of naturally occurring variants in these Ca+cycling genes, which may serve as prognostic or diagnostic factors as well as modifiers of heart failure development, is also discussed.

KW - Calcium

KW - Contractility

KW - Heart Failure

KW - Human Variants

KW - Sarcoplasmic Reticulum

UR - http://www.scopus.com/inward/record.url?scp=84944526498&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84944526498&partnerID=8YFLogxK

U2 - 10.1007/9783319087986_12

DO - 10.1007/9783319087986_12

M3 - Chapter

AN - SCOPUS:84944526498

SN - 9783319087986

SN - 9783319087979

SP - 205

EP - 215

BT - Introduction to Translational Cardiovascular Research

PB - Springer International Publishing

ER -