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


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

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

  • 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.