Rho-kinase inhibition reverses impaired Ca2+ handling and associated left ventricular dysfunction in pressure overload-induced cardiac hypertrophy

Olgar, YUSUF; Celen, MURAT; Yamasan, BİLGE; Ozturk, NİHAL; TURAN, Belma; ÖZDEMİR, SEMİR

doi:10.1016/j.ceca.2017.09.002

Rho-kinase inhibition reverses impaired Ca2+ handling and associated left ventricular dysfunction in pressure overload-induced cardiac hypertrophy

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Olgar Y., Celen M. C., Yamasan B. E., Ozturk N., TURAN B., ÖZDEMİR S.

CELL CALCIUM, vol.67, pp.81-90, 2017 (SCI-Expanded)

Publication Type: Article / Article
Volume: 67
Publication Date: 2017
Doi Number: 10.1016/j.ceca.2017.09.002
Journal Name: CELL CALCIUM
Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
Page Numbers: pp.81-90
Keywords: Cardiac hypertrophy, Rho kinases, Contractility, Calcium, Fasudil, Myocyte, CHANNEL RYANODINE RECEPTOR, INDUCED HEART-FAILURE, PROTEIN-KINASE, RAT-HEART, HYPERTENSIVE-RATS, FAILING HEARTS, CONTRACTILE, PHOSPHORYLATION, CLEAVAGE, MYOCYTES
Akdeniz University Affiliated: Yes

Abstract

Recent studies have implicated a relationship between RhoA/ROCK activity and defective Ca2+ homeostasis in hypertrophic hearts. This study investigated molecular mechanism underlying ROCK inhibition-mediated cardioprotection against pressure overload-induced cardiac hypertrophy, with a focus on Ca2+ homeostasis.