AMPK, Mitochondrial Function, and Cardiovascular Disease

• Published in: International journal of molecular sciences Vol. 21; no. 14; p. 4987
• Main Authors: Wu, Shengnan, Zou, Ming-Hui
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 15.07.2020; MDPI
• Subjects: Adenosine diphosphate; Adenosine kinase; Adenosine monophosphate; Adenosine triphosphate; Adenosine Triphosphate - metabolism; AMP-Activated Protein Kinases - analysis; AMP-Activated Protein Kinases - metabolism; AMPK; Animals; ATP; Berberine; Cardiovascular disease; Cardiovascular diseases; Cardiovascular Diseases - metabolism; Cardiovascular Diseases - pathology; Cellular stress response; Crosstalk; Deoxyribonucleic acid; Diabetes; DNA; Energy; Energy Metabolism; Fuel gages; Glucose; Homeostasis; Humans; Hydrogen peroxide; Hypoxia; Intracellular; Intracellular signalling; Kinases; Metabolism; Metformin; Mitochondria; Mitochondria - metabolism; Mitochondria - pathology; mitochondrial function; Mitochondrial Turnover; Nitric oxide; Nitrogen dioxide; Oxidative stress; Phosphorylation; Protein kinase; Proteins; Reactive Oxygen Species - metabolism; Reagents; Resveratrol; Review; Statins; cardiovascular disease; AMPK; mitochondrial function
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms21144987

Adenosine monophosphate-activated protein kinase (AMPK) is in charge of numerous catabolic and anabolic signaling pathways to sustain appropriate intracellular adenosine triphosphate levels in response to energetic and/or cellular stress. In addition to its conventional roles as an intracellular energy switch or fuel gauge, emerging research has shown that AMPK is also a redox sensor and modulator, playing pivotal roles in maintaining cardiovascular processes and inhibiting disease progression. Pharmacological reagents, including statins, metformin, berberine, polyphenol, and resveratrol, all of which are widely used therapeutics for cardiovascular disorders, appear to deliver their protective/therapeutic effects partially via AMPK signaling modulation. The functions of AMPK during health and disease are far from clear. Accumulating studies have demonstrated crosstalk between AMPK and mitochondria, such as AMPK regulation of mitochondrial homeostasis and mitochondrial dysfunction causing abnormal AMPK activity. In this review, we begin with the description of AMPK structure and regulation, and then focus on the recent advances toward understanding how mitochondrial dysfunction controls AMPK and how AMPK, as a central mediator of the cellular response to energetic stress, maintains mitochondrial homeostasis. Finally, we systemically review how dysfunctional AMPK contributes to the initiation and progression of cardiovascular diseases via the impact on mitochondrial function.