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Fig. 2 | Clinical Epigenetics

Fig. 2

From: Air pollution-induced placental alterations: an interplay of oxidative stress, epigenetics, and the aging phenotype?

Fig. 2

An extended view of the air pollution-induced telomere-mitochondrial aging hypothesis. Our previous hypothesis showed that the presence of air pollution-induced ROS within cells induces DNA damage which leads to telomere shortening. Both DNA damage and telomere shortening are associated with increased levels of p53, which on its turn leads to increased mitochondrial dysfunction. Furthermore, disturbances in mitochondria can also increase cellular ROS production. We extended this view with epigenetic regulation. A dynamic regulation exists between epigenetic marks and TL. High trimethylated histones at the subtelomeric and telomeric region as well as high subtelomeric DNA methylation by DNMTs are a negative regulator of TL. Additionally, shortening of telomeres leads to a decrease in both histone trimethylation and subtelomeric DNA methylation and global DNA methylation (Alu, LINE-1). Furthermore, microRNAs might be involved through DICER1 regulation that is linked to DNMT expression and on its turn affects methylation processes of the genome and subtelomeric regions. Finally, miRNAs are also under the regulation of both DNA methylation and p53. Both p53 and DICER1 may be under regulation of ROS

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