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Review
. 2021 Aug 11;22(16):8649.
doi: 10.3390/ijms22168649.

Protective Effects of Flavonoids Against Mitochondriopathies and Associated Pathologies: Focus on the Predictive Approach and Personalized Prevention

Lenka Koklesova  1 , Alena Liskova  1 , Marek Samec  1 , Kevin Zhai  2 , Raghad Khalid Al-Ishaq  2 , Ondrej Bugos  3 , Miroslava Šudomová  4 , Kamil Biringer  1 , Martin Pec  5 , Marian Adamkov  6 , Sherif T S Hassan  7 , Luciano Saso  8 , Frank A Giordano  9 , Dietrich Büsselberg  2 , Peter Kubatka  5   10 , Olga Golubnitschaja  10   11
Affiliations
Review

Protective Effects of Flavonoids Against Mitochondriopathies and Associated Pathologies: Focus on the Predictive Approach and Personalized Prevention

Lenka Koklesova et al. Int J Mol Sci. .

Abstract

Multi-factorial mitochondrial damage exhibits a "vicious circle" that leads to a progression of mitochondrial dysfunction and multi-organ adverse effects. Mitochondrial impairments (mitochondriopathies) are associated with severe pathologies including but not restricted to cancers, cardiovascular diseases, and neurodegeneration. However, the type and level of cascading pathologies are highly individual. Consequently, patient stratification, risk assessment, and mitigating measures are instrumental for cost-effective individualized protection. Therefore, the paradigm shift from reactive to predictive, preventive, and personalized medicine (3PM) is unavoidable in advanced healthcare. Flavonoids demonstrate evident antioxidant and scavenging activity are of great therapeutic utility against mitochondrial damage and cascading pathologies. In the context of 3PM, this review focuses on preclinical and clinical research data evaluating the efficacy of flavonoids as a potent protector against mitochondriopathies and associated pathologies.

Keywords: anti-oxidant activity; cancer; cardiovascular disease; dysfunction; flavonoids; genoprotection; injury; mitochondrial function; mitochondrial impairment; mitochondriopathy; natural substances; neurodegeneration; patient stratification; phytochemicals; predictive preventive personalized medicine (PPPM/3PM); stress; tumorigenesis.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Processes involved in mitochondrial impairments and associated diseases. Abbreviations: ROS, reactive oxygen species; RNS, reactive nitrogen species; mtDNA, mitochondrial DNA; MELAS, mitochondrial encephalomyopathy, lactic acidosis, and strokelike episode syndrome; CPEO, chronic progressive external ophthalmoplegia; CVDs, cardiovascular diseases; NOS, nitric oxide synthase; NO, nitric oxide; ONOO, peroxynitrite; ADP, adenosine diphosphate; ATP, adenosine triphosphate; MUTYH, mutY DNA glycosylase; SMUG1, single-strand selective monofunctional uracil-DNA glycosylase; APE1, human apurinic/apyrimidinic endonuclease; POL γ, DNA polymerase subunit gamma; NTH1, Nth like DNA glycosylase 1; OGG1, 8-oxoguanine DNA glycosylase; NEIL, human endonuclease VIII-like; PNKP, polynucleotide kinase 3′-phosphatase; O2, dioxygen; O2-, ion superoxide; H2O, dihydrogen monoxide/water.
Figure 2
Figure 2
Chemical structures and key representatives of the six major flavonoid classes.
Figure 3
Figure 3
The mechanisms of flavonoids in the prevention and treatment of mitochondriopathies. Abbreviations: EGCG, epigallocatechin-3-gallate; EGb 761®, Ginkgo biloba extract; CVDs, cardiovascular diseases; mtDNA, mitochondrial DNA; OXPHOS, oxidative phosphorylation; ROS, reactive oxygen species; ↑, increase/induce; ↓, decrease/reduce; ETC, electron transport chain.
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