Targeting Mitochondrial Biogenesis with Polyphenol Compounds

Abstract

Appropriate mitochondrial physiology is an essential for health and survival. Cells have developed unique mechanisms to adapt to stress circumstances and changes in metabolic demands, by meditating mitochondrial function and number. In this context, sufficient mitochondrial biogenesis is necessary for efficient cell function and haemostasis, which is dependent on the regulation of ATP generation and maintenance of mitochondrial DNA (mtDNA). These procedures play a primary role in the processes of inflammation, aging, cancer, metabolic diseases, and neurodegeneration. Polyphenols have been considered as the main components of plants, fruits, and natural extracts with proven therapeutic effects during the time. These components regulate the intracellular pathways of mitochondrial biogenesis. Therefore, the current review is aimed at representing an updated review which determines the effects of different natural polyphenol compounds from various plant kingdoms on modulating signaling pathways of mitochondrial biogenesis that could be a promising alternative for the treatment of several disorders.

Figure 1

The role of different signaling pathways in mitochondrial biogenesis.

Figure 2

Immunohistochemistry and ratio of Nrf2 in mouse brain 24 h after traumatic brain injury in different groups ((a) sham, (b) traumatic brain injury, (c) traumatic brain injury with vehicle, (d) effect of quercetin on the concentration of Nrf2 in the nucleus, and (e) significant increase in the ratio of Nrf2 in the quercetin group in compared with the traumatic brain injury/vehicle group). Data represent the mean ± SEM (n = 5 per group). Scale (20 μm). Reproduced under the terms and conditions of the Creative Commons Attribution 4.0 International License. Copyright 2016, PLOS [67].

Figure 3

Alteration in ultrastructural and mass of adipocyte mitochondria induced by hydroxytyrosol treatments (1.0 μM for 48 h). (a) Upsurge in the fluorescence intensity in MitoTracker staining. (b) Significant change (p < 0.01) in mitochondrial surface area and density in morphometric analysis using electron microscopy. (c) Electron microscope comparison of mitochondrial profiles (A, B) (magnification ×2110) and (C, D) (magnification ×11,000). Reproduced with permission of Elsevier [83].

Figure 4

Improvement of exercise performance and skeletal muscle mitochondrial biogenesis of mice using tangeretin. Hanging wire test (a, b), exercise tolerance test (c, d), transmission electron microscope micrographs (e), and mitochondrial numbers (f). Con (control), TG25 (25 mg/kg tangeretin group), TG50 (50 mg/kg tangeretin group), and TG100 (100 mg/kg tangeretin group) (mean ± SD), ^∗p < 0.05, ^∗∗p < 0.01 in comparison with the control group. Scale bars = 1 μm. Reprinted (adapted) with permission from [112]. Copyright (2018) American Chemical Society.