Activation of Histone Deacetylase-6 Induces Contractile Dysfunction Through Derailment of α-Tubulin Proteostasis in Experimental and Human Atrial Fibrillation
Author(s) -
Deli Zhang,
Chia-Tung Wu,
Xiaoyan Qi,
Roelien A. M. Meijering,
Femke HoogstraBerends,
Artavazd Tadevosyan,
Günseli Çubukçuoğlu Deniz,
Serkan Durdu,
Ahmet Rüçhan Akar,
Ody C.M. Sibon,
Stanley Nattel,
Robert H. Henning,
Bianca J.J.M. Brundel
Publication year - 2013
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.113.005300
Subject(s) - hdac6 , proteostasis , acetylation , medicine , histone deacetylase , histone deacetylase inhibitor , contractility , microbiology and biotechnology , microtubule , hdac4 , cancer research , pharmacology , histone , biology , biochemistry , gene
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.
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