Abstract:
BACKGROUND:Atrial remodeling in the form of fibrosis is considered the basis in the development of atrial fibrillation (AF). The aim of this study was to investigate the effects of doxycycline on atrial remodeling induced by chronic intermittent hypoxia (CIH) and the mechanisms underlying such changes. METHODS:A total of 45 Sprague-Dawley rats were randomized into three groups: control group, CIH group, CIH with doxycycline treatment (CIH-D) group. A rat model of atrial remodeling was established by CIH and Masson staining was used to evaluate the extent of atrial fibrosis. We studied the expression levels of microRNA-1 (miR-1), microRNA-21 (miR-21), microRNA-29b (miR-29b), microRNA-30 (miR-30), microRNA-133a (miR-133a), microRNA-328 (miR-328), transforming growth factor-β1 (TGF-β1), and connective tissue growth factor (CTGF). Atrial effective refractory period and AF inducibility were examined via isolated heart models of cardiac electrophysiology. RESULTS:Compared with the control rats, CIH rats showed higher atrial interstitial collagen deposition, increased AF inducibility, and increased miR-1, miR-21, miR-133a, miR-328, TGF-β1, and CTGF levels. Treatment with doxycycline significantly attenuated CIH-induced atrial fibrosis, improved AF inducibility, and reduced miR-1, miR-21, miR-133a, miR-328, TGF-β1, and CTGF. CONCLUSION:CIH induced significant atrial remodeling, which was attenuated by doxycycline in our rat model. These changes can be explained by the alterations initiated in the miR-133a/TGF-β1/CTGF pathway by doxycycline.
journal_name
Herzjournal_title
Herzauthors
Zhang K,Ma Z,Wang W,Liu R,Zhang Y,Yuan M,Li Gdoi
10.1007/s00059-018-4768-1subject
Has Abstractpub_date
2020-11-01 00:00:00pages
668-675issue
7eissn
0340-9937issn
1615-6692pii
10.1007/s00059-018-4768-1journal_volume
45pub_type
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