Chronic Non-Communicable Diseases (NCDs) have been considered a global health problem, characterized as diseases of multiple factors, which are developed throughout life, and regardless of genetics as a risk factor of important relevance, the increase in mortality attributed to the disease to environmental factors and the lifestyle one leads. Although the reactive species (ROS/RNS) are necessary for several physiological processes, their overproduction is directly related to the pathogenesis and aggravation of NCDs. In contrast, dietary polyphenols have been widely associated with minimizing oxidative stress and inflammation. In addition to their antioxidant power, polyphenols have also drawn attention for being able to modulate both gene expression and modify epigenetic alterations, suggesting an essential involvement in the prevention and/or development of some pathologies. Therefore, this review briefly explained the mechanisms in the development of some NCDs, followed by a summary of some evidence related to the interaction of polyphenols in oxidative stress, as well as the modulation of epigenetic mechanisms involved in the management of NCDs.
Keywords: 8-oxodG, 8-oxo-2́deosyguanosine; ABCG, ATP Binding Cassette Subfamily G Member; ADAM10, α-secretase; ADRB3, adrenoceptor Beta 3; APP, amyloid-β precursor protein; ARF, auxin response factor; ARH-I, aplysia ras homology member I; ARHGAP24, Rho GTPase Activating Protein 24; ATF6, activating transcription factor 6; ATP2A3, ATPase Sarcoplasmic/Endoplasmic Reticulum Ca2+ Transporting 3; BCL2L14, apoptosis facilitator Bcl-2-like protein 14; Bioactive compounds; CDH1, cadherin-1; CDKN, cyclin dependent kinase inhibitor; CPT, carnitine palmitoyltransferase; CREBH, cyclic AMP-responsive element-binding protein H; DANT2, DXZ4 associated non-noding transcript 2, distal; DAPK1, death-associated protein kinase 1; DNA methylation; DNMT, DNA methyltransferase; DOT1L, disruptor of telomeric silencing 1-like; EWASs, epigenome-wide association studies; EZH2, Enhancer of zeste homolog 2; FAS, Fas cell Surface Death Receptor; GDNF, glial cell line-derived neurotrophic factor; GFAP, glial fibrillary acid protein; GSTP1, Glutathione S-transferases P1; Gut microbiota modulation; HAT, histone acetylases; HDAC, histone deacetylases; HSD11B2, 11 beta-hydroxysteroid dehydrogenase type 2; Histone modifications; IGFBP3, insulin-like growth factor-binding protein 3; IGT, impaired glucose tolerance; KCNK3, potassium two pore domain channel subfamily K Member 3; MBD4, methyl-CpG binding domain 4; MGMT, O-6-methylguanine-DNA methyltransferase; NAFLD, Non-alcoholic fatty liver disease; OCT1, Organic cation transporter 1; OGG1, 8-Oxoguanine DNA Glycosylase; Oxidative stress; PAI-1, plasminogen activator inhibitor 1; PHOSPHO1, Phosphoethanolamine/Phosphocholine Phosphatase 1; PLIN1, perilipin 1; POE3A, RNA polymerase III; PPAR, peroxisome proliferator-activated receptor; PPARGC1A, PPARG coactivator 1 alpha; PRKCA, Protein kinase C alpha; PTEN, phosphatase and tensin homologue; Personalized nutrition; RASSF1A, Ras association domain family member 1; SAH, S -adenosyl-l-homocysteine; SAM, S-adenosyl-methionine; SD, sleep deprivation; SOCS3, suppressor of cytokine signaling 3; SREBP-1C, sterol-regulatory element binding protein-1C; TBX2, t-box transcription factor 2; TCF7L2, transcription factor 7 like 2; TET, ten-eleven translocation proteins; TNNT2, cardiac muscle troponin T; TPA, 12-O-tetradecanoylphorbol-13-acetate; lncRNA, long non-coding RNA; ncRNA, non-coding RNA; oAβ-induced-LTP, oligomeric amyloid-beta induced long term potentiation.
© 2022 The Author(s).