Abstract
A large number of diverse mechanisms that lead to cytoprotection have been described to date. Perhaps, not surprisingly, the role of mitochondria in these phenomena is notable. In addition to being metabolic centers, due to their role in cell catabolism, ATP synthesis, and biosynthesis these organelles are triggers and/or end-effectors of a large number of signaling pathways. Their role in the regulation of the intrinsic apoptotic pathway, calcium homeostasis, and reactive oxygen species signaling is well documented. In this review, we aim to characterize the prospects of influencing cytoprotective mitochondrial signaling routes by natural substances of plant origin, namely, flavonoids (e.g., flavanones, flavones, flavonols, flavan-3-ols, anthocyanidins, and isoflavones). Flavonoids are a family of widely distributed plant secondary metabolites known for their beneficial effects on human health and are widely applied in traditional medicine. Their pharmacological characteristics include antioxidative, anticarcinogenic, anti-inflammatory, antibacterial, and antidiabetic properties. Here, we focus on presenting mitochondria-mediated cytoprotection against various insults. Thus, the role of flavonoids as antioxidants and modulators of antioxidant cellular response, apoptosis, mitochondrial biogenesis, autophagy, and fission and fusion is reported. Finally, an emerging field of flavonoid-mediated changes in the activity of mitochondrial ion channels and their role in cytoprotection is outlined.
Highlights
Different forms of cell death have been implicated in the pathogenesis of many human diseases
Our aim is to concentrate on the modulation of mitochondrial function by flavonoids, which leads to cytoprotection and the possible application of these chemicals as pharmacological agents
Enzymes involved in this regulation of cellular redox status and protection against oxidative damage include glutathione-S-transferase (GST), hemeoxygenase 1 (HO-1) and NADPH:quinone oxidoreductase 1 (NQO1)
Summary
Different forms of cell death (i.e., apoptosis, necroptosis, ferroptosis, and necrosis) have been implicated in the pathogenesis of many human diseases. The death of neuronal cells is implicated in the neurogenerative diseases Alzheimer’s and Parkinson’s disease, both of which have shown increasing prevalence in aging populations [5,6]. It has been shown that the level of dietary flavonoid consumption correlates with the reduced risk of many. Extensive studies have shown that flavonoids have antioxidant [14,15], metal chelation [16,17], signal transduction, gene expression, and enzyme function modulating properties [18]. A recent meta-analysis demonstrated that dietary intake of anthocyanins reduced the risk of coronary heart disease and cardiovascular disease mortality [30]. The results by Shishtar et al suggest that higher long-term consumption of flavonoids in the diet lowers the risk of Alzheimer’s disease development in adults [34]. Our aim is to concentrate on the modulation of mitochondrial function by flavonoids, which leads to cytoprotection and the possible application of these chemicals as pharmacological agents
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