Abstract
Mitochondrial dysfunction may play a crucial role in various diseases due to its roles in the regulation of energy production and cellular metabolism. Serine/threonine kinase (AKT) is a highly recognized antioxidant, immunomodulatory, anti-proliferation, and endocrine modulatory molecule. Interestingly, increasing studies have revealed that AKT can modulate mitochondria-mediated apoptosis, redox states, dynamic balance, autophagy, and metabolism. AKT thus plays multifaceted roles in mitochondrial function and is involved in the modulation of mitochondria-related diseases. This paper reviews the protective effects of AKT and its potential mechanisms of action in relation to mitochondrial function in various diseases.
Highlights
Mitochondria have become a hot research topic due to their important roles in the physiological regulation of the body
Mitochondrial function may be related to the formation of diseases through a variety of mechanisms including the production of oxidative stress, apoptosis, and cell division, fusion, and mitosis [6]
The activation of AKT promotes the stabilization of NFE2-related nuclear factor (NRF) 2 via the inhibition of glycogen synthase kinase 3β (GSK3β) and accumulation of cyclin-dependent kinase inhibitor 1A, which inhibits the binding of kelch-like ECH-associated protein 1 (KEAP1) to NRF2.The accumulated NRF2 is translocated to the nucleus, thereby activating several antioxidant genes including those related to glutathione biosynthesis such as glutamine cysteine ligase catalytic subunit, glutamine cysteine ligase modifier subunit, and glutathione oxidase, as well as other enzymes that are able to reduce and use the protein antioxidant thioredoxin to control cellular reactive oxygen species (ROS) production [74]
Summary
Mitochondria have become a hot research topic due to their important roles in the physiological regulation of the body. Mitochondrial function may be related to the formation of diseases through a variety of mechanisms including the production of oxidative stress, apoptosis, and cell division, fusion, and mitosis [6]. AKT and mitochondria-related diseases effective DNA repair mechanisms and the mitochondrial DNA is not shielded from oxidative stress by histones [17, 18]. AKT is the core of many signaling pathways and is usually suppressed in many types of mitochondrial dysfunction, and as such, activation of AKT can maintain the normal function of mitochondria in several disease states [28, 29]. This review may provide a new focus for the therapy of mitochondrial functionrelated diseases
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