Τίτλος:
AMP-activated protein kinase: A remarkable contributor to preserve a healthy heart against ROS injury
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Heart failure is one of the leading causes of death and disability worldwide. Left ventricle remodeling, fibrosis, and ischemia/reperfusion injury all contribute to the deterioration of cardiac function and predispose to the onset of heart failure. Adenosine monophosphate-activated protein kinase (AMPK) is the universally recognized energy sensor which responds to low ATP levels and restores cellular metabolism. AMPK activation controls numerous cellular processes and, in the heart, it plays a pivotal role in preventing onset and progression of disease. Excessive reactive oxygen species (ROS) generation, known as oxidative stress, can activate AMPK, conferring an additional role of AMPK as a redox-sensor. In this review, we discuss recent insights into the crosstalk between ROS and AMPK. We describe the molecular mechanisms by which ROS activate AMPK and how AMPK signaling can further prevent heart failure progression. Ultimately, we review the potential therapeutic approaches to target AMPK for the treatment of cardiovascular disease and prevention of heart failure. © 2021 The Author(s)
Συγγραφείς:
Marino, A.
Hausenloy, D.J.
Andreadou, I.
Horman, S.
Bertrand, L.
Beauloye, C.
Περιοδικό:
FREE RADICAL BIOLOGY AND MEDICINE
Εκδότης:
W B SAUNDERS CO-ELSEVIER INC
Λέξεις-κλειδιά:
adenosine triphosphate; calcium calmodulin dependent protein kinase kinase; calcium calmodulin dependent protein kinase kinase beta; catalase; cystathionine beta synthase; dipeptidyl carboxypeptidase; endothelial nitric oxide synthase; glutathione peroxidase; hydroxymethylglutaryl coenzyme A reductase inhibitor; hydroxymethylglutaryl coenzyme A reductase kinase; inducible nitric oxide synthase; mammalian target of rapamycin complex 1; metformin; peroxisome proliferator activated receptor gamma; peroxisome proliferator activated receptor gamma coactivator 1alpha; phosphatidylinositol 3 kinase; pioglitazone; protein kinase C; protein kinase LKB1; Rac1 protein; Rac2 protein; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide phosphate oxidase; reduced nicotinamide adenine dinucleotide phosphate oxidase 1; reduced nicotinamide adenine dinucleotide phosphate oxidase 2; reduced nicotinamide adenine dinucleotide phosphate oxidase 3; reduced nicotinamide adenine dinucleotide phosphate oxidase 4; resveratrol; rosiglitazone; sirtuin 1; small interfering RNA; superoxide dismutase; unclassified drug; adenosine phosphate; hydroxymethylglutaryl coenzyme A reductase kinase; reactive oxygen metabolite, AMPK signaling; cardiac muscle cell; cell growth; cell proliferation; disease course; endothelium cell; enzyme activation; enzyme inhibition; enzyme regulation; heart failure; heart mitochondrion; heart protection; heart ventricle hypertrophy; human; in vitro study; nonhuman; oxidative stress; phagocyte; protein expression; protein function; protein phosphorylation; protein targeting; reperfusion injury; Review; thrombosis; vascular smooth muscle cell; cardiac muscle; genetics, Adenosine Monophosphate; AMP-Activated Protein Kinases; Myocardium; Myocytes, Cardiac; Reactive Oxygen Species
DOI:
10.1016/j.freeradbiomed.2021.02.047
