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, cilt.67, ss.81-90, 2017 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 67
  • Basım Tarihi: 2017
  • Doi Numarası: 10.1016/j.ceca.2017.09.002
  • Dergi Adı: CELL CALCIUM
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.81-90
  • Anahtar Kelimeler: 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 Üniversitesi Adresli: Evet

Özet

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.