Activation of Histone Deacetylase-6 Induces Contractile Dysfunction Through Derailment of alpha-Tubulin Proteostasis in Experimental and Human Atrial Fibrillation

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Zhang D., Wu C., Qi X., Meijering R. A. M., Hoogstra-Berends F., Tadevosyan A., ...Daha Fazla

CIRCULATION, cilt.129, sa.3, ss.346-358, 2014 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 129 Sayı: 3
  • Basım Tarihi: 2014
  • Doi Numarası: 10.1161/circulationaha.113.005300
  • Dergi Adı: CIRCULATION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.346-358
  • Anahtar Kelimeler: alpha-tubulin deacetylase, atrial fibrillation, Drosophila, epigenesis, genetic, HDAC6 protein, Drosophila, HDAC6 protein, human, MICROTUBULE DISRUPTION, THERAPEUTIC TARGETS, STRUCTURAL-CHANGES, HDAC6 INHIBITOR, DISEASE, HEART, CYTOSKELETON, ACETYLATION, DEGRADATION, PROTEOLYSIS
  • Ankara Üniversitesi Adresli: Evet

Özet

Background Atrial fibrillation (AF) is characterized by structural remodeling, contractile dysfunction, and AF progression. Histone deacetylases (HDACs) influence acetylation of both histones and cytosolic proteins, thereby mediating epigenetic regulation and influencing cell proteostasis. Because the exact function of HDACs in AF is unknown, we investigated their role in experimental and clinical AF models.