AMP-Activated Protein Kinase α1 Regulates Cardiac Gap Junction Protein Connexin 43 and Electrical Remodeling Following Pressure Overload
Author(s) -
Ioana Alesutan,
Jakob Voelkl,
Florian Stöckigt,
Sobuj Mia,
Martina Feger,
Uwe Primeßnig,
Mentor Sopjani,
Carlos Muñoz,
Oliver Borst,
Meinrad Gawaz,
Burkert Pieske,
Bernhard Metzler,
Frank R. Heinzel,
Jan W. Schrickel,
Florian Läng
Publication year - 2015
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000369706
Subject(s) - ampk , connexin , protein kinase a , pressure overload , medicine , endocrinology , chemistry , microbiology and biotechnology , amp activated protein kinase , gap junction , phosphorylation , biology , muscle hypertrophy , intracellular , cardiac hypertrophy
Adenosine 5'-monophosphate (AMP)-activated protein kinase (Ampk) modulates a wide array of cellular functions and regulates various ion channels and transporters. In failing human hearts an increased Ampkα1 activity was observed. The present study aimed to uncover the impact of Ampkα1 on cardiac electrical remodeling.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom