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MitoQ for vitiligo by mitigating PARP1 translocation aberrations: Network pharmacology and experimental validation
Renxue Xiong1, Shiyu Jin2, Yujie Li2
1Hangzhou Third Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, China; Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China.
Purpose:
Oxidative stress plays a significant role in the development of vitiligo. Although the specific mechanism of the mitochondria-targeted antioxidant mitoquinone (MitoQ) in vitiligo remains unclear, it has shown promise in the treatment of various diseases.
Methods:
In this study, we employed network pharmacology, molecular docking, transcriptomic approaches, and experimental verification to investigate the potential targets of MitoQ in vitiligo.
Results:
Molecular docking results identified four possible crucial targets of MitoQ in vitiligo treatment: poly (ADP-ribose) polymerase 1 (PARP1), prostaglandin-endoperoxide synthase 2 (PTGS2), estrogen receptor 1 (ESR1), and C-X-C motif chemokine receptor 3 (CXCR3). MitoQ alleviated oxidative stress-induced PARP1 nuclear mislocalization, attenuated ROS accumulation, restored mitochondrial membrane potential, and enhanced ATP synthesis in vitro analysis. Transcriptomic analysis demonstrated that MitoQ reduced the expression of DNA damage genes and genes involved in the PI3K-AKT and MAPK signaling pathways. The protein-protein interaction network indicated a potential relationship between PARP1 and DNA damage-related genes, suggesting that MitoQ could interfere with abnormal PARP1 activation. Notably, MitoQ reduced cellular senescence by decreasing CDKN1A/p21 protein through PARP1, and the knockdown of PARP1 reduced oxidative damage.
Conclusion:
These results indicate that PARP1 decreases cellular senescence and offers a potential target for therapeutic research in the management of vitiligo.
Insights
Mitoquinone (MitoQ) may treat vitiligo by targeting poly (ADP-ribose) polymerase 1 (PARP1), reducing oxidative stress and cellular senescence. This research identifies PARP1 as a key therapeutic target for vitiligo management.
Area of Science:
- Dermatology and Molecular Medicine
- Investigating the molecular mechanisms of skin diseases
- Exploring novel therapeutic targets for autoimmune disorders
Background:
- Oxidative stress is a key factor in vitiligo pathogenesis.
- Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, shows therapeutic potential in various diseases.
- The precise role of MitoQ in vitiligo treatment requires elucidation.
Purpose of the Study:
- To investigate the potential molecular targets of MitoQ in vitiligo.
- To explore the therapeutic mechanisms of MitoQ in vitiligo.
- To identify novel therapeutic strategies for vitiligo.
Main Methods:
- Network pharmacology and molecular docking to identify MitoQ targets.
- Transcriptomic analysis to assess gene expression changes.
- In vitro experiments to validate MitoQ's effects on oxidative stress and cellular senescence.
Main Results:
- Identified poly (ADP-ribose) polymerase 1 (PARP1) as a crucial target of MitoQ in vitiligo.
- MitoQ alleviated oxidative stress, restored mitochondrial function, and reduced DNA damage-related gene expression.
- MitoQ decreased cellular senescence by downregulating CDKN1A/p21 via PARP1, and PARP1 knockdown reduced oxidative damage.
Conclusions:
- PARP1 plays a significant role in mitigating cellular senescence in vitiligo.
- Targeting PARP1 with MitoQ presents a promising therapeutic avenue for vitiligo.
- Further research into PARP1-mediated mechanisms could lead to effective vitiligo treatments.
