Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Volume 1852, Issue 2, February 2015, Pages 232-242
ReviewInterplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic cardiomyopathy☆
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Abbreviations
AGEs
advanced glycosylation end products
AMPK
AMP-activated protein kinase
AT1R receptor
angiotensine II receptor type 1
CaMKII
Ca2 +/calmodulin-dependent protein kinase II
CB1/2 receptor
cannabinoid 1 and 2 receptors
eNOS
endothelial nitric oxide synthase
ER stress
endoplasmatic reticulum stress
ICAM-1
intercellular adhesion molecule 1, also known as CD54
iNOS
inducible nitric oxide synthase
MAPKs
mitogen activated protein kinases
MCP-1
monocyte chemoatractic protein-1
MMPs
matrix metalloproteinases
mTOR
mammalian target of rapamycin
NADPH oxidase/NOX
nicotinamide adenine dinucleotide phosphate-oxidase
NFkB
nuclear factor kappaB
NO
nitric oxide
NOS
nitric oxide synthases
Nrf2
NFE2L2 nuclear factor, erythroid 2-like 2
PARP-1
poly(ADP)ribose polymerase 1
PARP-1
poly(ADP-ribose) polymerase 1
RAGE
receptor for advanced glycation end product
ROS/RNS
reactive oxygen and nitrogen species
SERCA2a
sarco/endoplasmic reticulum Ca2 +-ATPase
STZ
streptozotocin
VCAM-1
vascular cell adhesion molecule 1, also known as CD106
XO
xanthine oxidase/oxidoreductase.
Keywords
Diabetic cardiomyopathy
Protein oxidation
Autophagy
Oxidative stress
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This article is part of a Special Issue entitled: Autophagy and protein quality control in cardiometabolic diseases.
Published by Elsevier B.V.