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., ...More

CIRCULATION, vol.129, no.3, pp.346-358, 2014 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 129 Issue: 3
  • Publication Date: 2014
  • Doi Number: 10.1161/circulationaha.113.005300
  • Journal Name: CIRCULATION
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.346-358
  • Keywords: 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 University Affiliated: Yes

Abstract

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.