Cardiac-specific overexpression of E40K active Akt prevents pressure overload-induced heart failure in mice by increasing angiogenesis and reducing apoptosis.
Ceci
M
M
Gallo
P
P
Santonastasi
M
M
Grimaldi
S
S
Latronico
M V G
MV
Pitisci
A
A
Missol-Kolka
E
E
Scimia
M C
MC
Catalucci
D
D
Hilfiker-Kleiner
D
D
Condorelli
G
G
D000818:Animals; D017209:Apoptosis; D001794:Blood Pressure; D002303:Cardiac Output, Low / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D003326:Coronary Circulation; D005786:Gene Expression Regulation; D018698:Glutamic Acid / Q000235:genetics*; D008239:Lysine / Q000235:genetics*; D051379:Mice; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000473:pathology; D018919:Neovascularization, Physiologic; D051057:Proto-Oncogene Proteins c-akt / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism
D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D018698:Glutamic Acid; D051057:Proto-Oncogene Proteins c-akt; D008239:Lysine