LncRNA AW112010 Promotes Mitochondrial Biogenesis and Hair Cell Survival: Implications for Age-Related Hearing Loss

Figure 8

Schematic model demonstrating that activated Arid5b/AW112010 signaling promotes mitochondrial biogenesis in the cochlea. Oxidative stress, mitochondrial DNA (mtDNA) mutations, decreased autophagy, and microRNA disorder account for the death of cochlear hair cells [1, 2, 4, 5]. During aging, adverse factors such as oxidative stress and energy shortage result in the dysregulation of cochlear lncRNAs, which might have protective or harmful roles in cochlear cell survival. In these adverse conditions, transcription factor Arid5b is elevated and activates the expression of AW112010. AW112010, probably via the activation of AMPK, increases the expression of PGC-1α and TFAM and promotes mitochondrial biogenesis (MB) in the purpose of protecting the cochlear hair cell from death.