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Aging and disease    2020, Vol. 11 Issue (4) : 967-977     DOI: 10.14336/AD.2019.0901
Review |
Targeting AMP-Activated Protein Kinase in Aging-Related Cardiovascular Diseases
Li Tian1, Mu Nan1, Yin Yue1, Yu Lu2,*, Ma Heng1,*
1Department of physiology and pathophysiology, School of Basic Medicine, Fourth Military Medical University, Xi'an, China
2Department of pathology, Xijing Hospital, Fourth Military Medical University, Xi’an, China
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Abstract  

Aging is a pivotal risk factor for developing cardiovascular diseases (CVD) due to the lifelong exposure to various risk factors that may affect the heart and vasculature during aging. AMP-activated protein kinase (AMPK), a serine/threonine protein kinase, is a pivotal endogenous energy regulator that protects against various pathological alterations. In this report, we first introduced the protective mechanisms of AMPK signaling in myocardium, such as oxidative stress, apoptosis, inflammation, autophagy and inflammatory response. Next, we introduced the potential correlation between AMPK and cardiac aging. Then, we highlighted the roles of AMPK signaling in cardiovascular diseases, including myocardial ischemia, cardiomyopathy, and heart failure. Lastly, some potential directions and further perspectives were expanded. The information extends our understanding on the protective roles of AMPK in myocardial aging, which may contribute to the design of drug targets and sheds light on potential treatments of AMPK for aging-related CVD.

Keywords AMPK      Aging      Cardiovascular diseases      Cardioprotecion     
Corresponding Authors: Yu Lu,Ma Heng   
About author:

These authors contributed equally to this work.

Just Accepted Date: 27 January 2020   Issue Date: 30 July 2020
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Li Tian
Mu Nan
Yin Yue
Yu Lu
Ma Heng
Cite this article:   
Li Tian,Mu Nan,Yin Yue, et al. Targeting AMP-Activated Protein Kinase in Aging-Related Cardiovascular Diseases[J]. Aging and disease, 2020, 11(4): 967-977.
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http://www.aginganddisease.org/EN/10.14336/AD.2019.0901     OR
ModelsRegulationEffectsReferences
C57BL/6 miceOxidative stressFGF19 activates AMPK to prevent ROS production protect the diabetic cardiomyocytes from oxidative stress induced damageLi et al. (2018) [14]
H9C2 cells / Diabetic miceOxidative stress and InflammationFortunellin protects against fructose-induced inflammation and oxidative stress by enhancing AMPK/Nrf2 pathwayZhao et al. (2017) [16]
Sprague-Dawley ratsOxidative stress and ApoptosisPterostilbene activates AMPK to suppress cardiac oxidative stress and apoptosisKosuru et al. (2018) [17]
Neonatal rat cardiomyocytesOxidative stressResveratrol inhibits ROS production by increasing phosphorylation of AMPKGuo et al. (2015) [19]
H9C2 cells/C57BL/6 miceOxidative stress and ApoptosisMelatonin inhibits apoptosis and oxidative stress via the activation of AMPK and upregulation of PGC1α with its downstream signalingLiu et al. (2018) [33]
H9c2 cellsAutophagyAMPK restores autophagy and protects against cardiac apoptosis.He et al. (2013) [39]
FNDC5(irisin-precursor) homozygous knockout (FNDC5-KO) mice / Cardiomyocytes from neonatal Sprague-Dawley ratsAutophagyIrisin protects against cardiac hypertrophy by inducing protective autophagy and autophagy flux via activating AMPK-ULK1 signalingLi et al. (2018) [41]
APN knockout (APNKO) miceApoptosis and InflammationAdiponectin knockout exacerbates LPS-induced cardiac dysfunctionRen et al. (2016) [56]
H9c2 cellsInflammationAMPK activation inhibits mRNA and protein levels of pro-inflammatory cytokines, such as TNF-α and IL-6Chen et al. (2018) [54]
Table 1  Protective mechanisms of AMPK signaling in myocardium.
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