AMP-activated protein kinase: A remarkable contributor to preserve a healthy heart against ROS injury

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.

Automated summary

Heart failure is a major cause of death and disability globally, with left ventricular remodeling, fibrosis, and ischemia/reperfusion injury contributing to cardiac dysfunction. AMPK acts as a universal energy sensor in response to low ATP levels, playing a crucial role in the heart. Excessive reactive oxygen species can activate AMPK, providing an additional role as a redox sensor for preventing heart failure progression.