Transient receptor potential canonical-3 channel-dependent fibroblast regulation in atrial fibrillation

Transient receptor potential canonical-3 channel-dependent fibroblast regulation in atrial fibrillation

TRPC3 channels regulate cardiac fibroblast proliferation and differentiation, likely by controlling the Ca(2+) influx that activates extracellular signal-regulated kinase signaling. AF increases TRPC3 channel expression by causing NFAT-mediated downregulation of microRNA-26 and causes TRPC3-dependen...

Teljes leírás

Elmentve itt :
Bibliográfiai részletek
Szerzők: Harada Masahide
Luo Xiaobin
Qi Xiao Yan
Tadevosyan Artavazd
Maguy Ange
Ördög Balázs
Ledoux Jonathan
Kato Takeshi
Naud Patrice
Voigt Niels
Shi Yanfen
Kamiya Kaichiro
Murohara Toyoaki
Kodama Itsuo
Tardif Jean-Claude
Schotten Ulrich
Van Wagoner David R.
Dobrev Dobromir
Nattel Stanley
Dokumentumtípus: Cikk
Megjelent: 2012-10-23
Sorozat:Circulation 126 No. 17
doi:10.1161/CIRCULATIONAHA.112.121830

mtmt:3079302
Online Access:http://publicatio.bibl.u-szeged.hu/9037
Leíró adatok
Tartalmi kivonat:TRPC3 channels regulate cardiac fibroblast proliferation and differentiation, likely by controlling the Ca(2+) influx that activates extracellular signal-regulated kinase signaling. AF increases TRPC3 channel expression by causing NFAT-mediated downregulation of microRNA-26 and causes TRPC3-dependent enhancement of fibroblast proliferation and differentiation. In vivo, TRPC3 blockade prevents AF substrate development in a dog model of electrically maintained AF. TRPC3 likely plays an important role in AF by promoting fibroblast pathophysiology and is a novel potential therapeutic target.
Terjedelem/Fizikai jellemzők:2051-2064
ISSN:1524-4539

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