Recently, effects on mitochondrial morphology and a critical role for mitochondrial homeostasis in PD has been attributed to the loss of PINK1 function, and it was suggested that the PD-associated proteins PINK1 and Parkin may act in the same pathway to modulate mitochondrial morphology [44], [47], [48].
Growing evidence shows that Bcl-2 family proteins also modulate mitochondrial morphology and cellular metabolism independently from cell death mechanisms.
Furthermore, Akt has also been recently shown to modulate mitochondrial morphology, but whether it does so in the context of ischaemic conditioning is not known (Ong et al., 2014; Parra et al., 2014).
Mitochondrial dysfunctions have been found to be associated with aging, several degenerative diseases, and cancer., Members of the BCL-2 apoptotic pathway have also been shown to modulate mitochondrial morphology.
Interestingly, some of the cardioprotective kinases, which have been linked to MPTP inhibition in the setting of ischaemic conditioning such as PKA (Sanada et al., 2004) and Akt, have been reported to modulate mitochondrial morphology through the phosphorylation of Drp1 (Chang and Blackstone, 2007; Cribbs and Strack, 2007) and OPA1 (Parra et al., 2014) respectively.
Our in silico analysis of Oxr1 binding partners identified RNA-post-transcriptional modification as a downstream function regulated by Oxr1-C, and given the known function of Fus and Tdp-43 as splicing regulators, we assessed the splicing of genes that modulate mitochondrial morphology and function.
An increasing number of genetically-engineered and aging rodent models are shedding additional light on the mitochondrion's role in regulating glucose metabolism and insulin sensitivity by modulating mitochondrial morphology, function and quality control pathways.
It could be possible that altered hnRNP A1 expression modulates mitochondrial morphology by controlling Drp1 expression in HD.
The authors proposed that an unknown function of the G72 in modulating mitochondrial morphology might be responsible for the risk-conferring property of the gene.
In addition, it was reported that HuR, a member of the ELAV family of RNA binding proteins directly binds to the 5′UTR of Bcl-xL mRNA, and that inhibition of HuR modulates mitochondrial morphology in U2OS cells [42].
Membrane prohibitin regulate the cellular signaling of membrane transport, nuclear prohibitin control transcription activation and the cell cycle, and mitochondrial prohibitin complex stabilize the mitochondrial genome and modulate mitochondrial dynamics, mitochondrial morphology, mitochondrial biogenesis, and the mitochondrial intrinsic apoptotic pathway.
