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Global Translational Medicine Influence of ferroptosis in neurological diseases
A B
Figure 8. Therapeutic drugs and miRNA that might target ferroptotic transcription factors (FerrTFs) for Parkinson’s disease (PD). (A) 633 drugs that
might be therapeutic against 6 FerrTFs for PD. (B) 114 miRNAs that might silence 5 FerrTFs against PD.
inflammatory processes, which trigger neuroinflammation neurodegeneration, daunorubicin may act against 5 common
and neurodegeneration . Our analysis suggests that FerrTFs, namely ATF4, MAPK3, MYB, TNFAIP3, and TP53,
[70]
FerrTFs induce inflammatory pathways through NF-κB in AD and PD. Regarding therapeutic miRNAs, our findings
signaling, contributing to neurodegeneration during PD. suggest that hsa-miR-132 could silence three common
FerrTFs for AD and PD, namely MYB, MAPK1, and MAPK3.
Thus, it can be asserted that FerrTFs influence the Literature supports miR-132’s multifarious neuroprotective
progression of neurological disorders such as AD and roles, and its decreased expression has been reported in post-
PD to a greater extent, warranting the development of mortem AD brains . These drugs and miRNAs represent
[72]
therapeutic measures targeting these FerrTFs. Accordingly, promising candidates for future experimental testing to
we have also devised therapeutic drugs and miRNAs that elucidate their potential in dampening ferroptosis during the
can be used to combat AD and PD. Among the drugs, we pathogenesis of AD and PD.
identified 592 drugs that commonly target FerrTFs found
in both neurodegenerative diseases. Notably, most of the 5. Conclusion
drugs are targeted against TP53, and the drugs citric acid In this study, we have unveiled the crosslink between
and daunorubicin are commonly implicated. Citric acid has ferroptosis, an iron-mediated cell death process, and
previously been shown to reduce oxidative stress in brain two neurodegenerative diseases, AD, and PD, using a
cells , and in our study, it was found to target two FerrTFs, network and systems biology approach. Our analyses
[71]
namely TP53 and HNF4A, in both AD and PD. While have demonstrated that the expression of a significant
there is no evidence pointing to its ability in preventing number of genes is modulated by ferroptosis-associated
Volume 2 Issue 3 (2023) 10 https://doi.org/10.36922/gtm.0318

