Glycogen Synthase Kinase-3α Limits Ischemic Injury, Cardiac Rupture, Post–Myocardial Infarction Remodeling and Death
Author(s) -
Hind Lal,
Jibin Zhou,
Firdos Ahmad,
Raihana Zaka,
Ronald J. Vagnozzi,
Morgan DeCaul,
James R. Woodgett,
Erhe Gao,
Thomas Force
Publication year - 2011
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.111.050666
Subject(s) - medicine , cardiology , myocardial infarction , ventricular remodeling , glycogen , gsk 3 , ischemic injury , glycogen synthase , ischemia , kinase , microbiology and biotechnology , biology
The molecular pathways that regulate the extent of ischemic injury and post-myocardial infarction (MI) remodeling are not well understood. We recently demonstrated that glycogen synthase kinase-3α (GSK-3α) is critical to the heart's response to pressure overload. However, the role, if any, of GSK-3α in regulating ischemic injury and its consequences is not known.
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