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. 2021 Nov 22;10(11):1854. doi: 10.3390/antiox10111854

Figure 11.

Figure 11

The proposed interplay between miR-15b-5p/miR-92b-3p and their target genes in the intermittent hypoxia with re-oxygenation (IHR) model of obstructive sleep apnea (OSA). (A) These interactions contribute to the development of depression by IHR-induced MAOA hyperactivity and IHR-induced oxidative stress/apoptosis/inflammation in OSA patients. (B) A schematic diaphragm depicts the protective effect of miR-15b-5p/miR-92b-3p mimics on IHR-induced oxidative stress and cell apoptosis through inhibiting MAOA via targeting PTGS1-NF-κB-SP1 signaling in OSA-related depression. IHR augments PTGS1, which increases the NF-κB expression that in turn activates MAOA gene transcription through augmenting the binding of SP1 to the promoter region of the MAOA gene. Down-regulation of miR-15b-5p/miR92b-3p in response to chronic IHR in OSA leads to MAOA hyperactivity, oxidative stress, and cell injury through targeting PTGS1-NF-κB1-SP1 signaling. MAOA = monoamine oxidase A; PTGS1 = prostaglandin-endoperoxide synthase 1; NF-κB1 = nuclear factor kappa B subunit 1; SP1 = Sp1 transcription factor.