Prx, short for peroxiredoxin, is a family of thiol-based peroxidases. They act as regulators of redox signaling, which is crucial for cell growth, metabolism, hormone signaling, and immune regulation. Prxs can function as antioxidants and chaperones, playing a vital role in maintaining cellular redox homeostasis [1].

Some members of the Prx family, like Prx I, are up-regulated under stress conditions. The transcription factor Nrf2 and its inhibitor Keap1 regulate stress-induced Prx I gene activation through the ARE/EpRE [6]. In the context of disease, mutations in the PRX gene, which encodes periaxins, can lead to Charcot-Marie-Tooth disease type 4F (CMT4F) [5]. Also, in non-small cell lung cancer, the PRX-1/TLR4 axis promotes hypoxia-induced radiotherapy resistance by targeting the NF-κB/p65 pathway [2]. In neurodegeneration, Prx II mitigates endoplasmic reticulum stress and mitochondrial dysfunction, and in osteoarthritis, Prx II reduces oxidative stress and cell senescence in chondrocytes by activating the p16-CDK4/6-pRb-E2F signaling pathway [3,4].

In conclusion, Prx is essential for redox signaling and stress response in cells. Studies on Prx in relation to various diseases such as CMT4F, non-small cell lung cancer, neurodegeneration, and osteoarthritis have provided insights into its functions. These findings from different disease-related research on Prx contribute to understanding its role in maintaining cellular health and the pathogenesis of multiple diseases.

References:

1. Mishra, Murli, Jiang, Hong, Wu, Lisha, Chawsheen, Hedy A, Wei, Qiou. 2015. The sulfiredoxin-peroxiredoxin (Srx-Prx) axis in cell signal transduction and cancer development. In Cancer letters, 366, 150-9. doi:10.1016/j.canlet.2015.07.002. https://pubmed.ncbi.nlm.nih.gov/26170166/

2. Hao, Jiaojiao, Song, Zhuo, Su, Jiayi, Zou, Lijian, Zou, Kun. 2023. The PRX-1/TLR4 axis promotes hypoxia-induced radiotherapy resistance in non-small cell lung cancer by targeting the NF-κB/p65 pathway. In Cellular signalling, 110, 110806. doi:10.1016/j.cellsig.2023.110806. https://pubmed.ncbi.nlm.nih.gov/37468052/

3. Jin, Mei-Hua, Feng, Lin, Xiang, Hong-Yi, Han, Ying-Hao, Kwon, Taeho. 2024. Exploring the role of Prx II in mitigating endoplasmic reticulum stress and mitochondrial dysfunction in neurodegeneration. In Cell communication and signaling : CCS, 22, 231. doi:10.1186/s12964-024-01613-x. https://pubmed.ncbi.nlm.nih.gov/38637880/

4. Shao, J-H, Fu, Q-W, Li, L-X, Peng, J-H, Chen, Y. . Prx II reduces oxidative stress and cell senescence in chondrocytes by activating the p16-CDK4/6-pRb-E2F signaling pathway. In European review for medical and pharmacological sciences, 24, 3448-3458. doi:10.26355/eurrev_202004_20802. https://pubmed.ncbi.nlm.nih.gov/32329817/

5. Ma, Xinran, Liu, Xiaoxuan, Duan, Xiaohui, Fan, Dongsheng. 2023. Screening for PRX mutations in a large Chinese Charcot-Marie-Tooth disease cohort and literature review. In Frontiers in neurology, 14, 1148044. doi:10.3389/fneur.2023.1148044. https://pubmed.ncbi.nlm.nih.gov/37470010/

6. Ishii, Tetsuro, Yanagawa, Toru. . Stress-induced peroxiredoxins. In Sub-cellular biochemistry, 44, 375-84. doi:. https://pubmed.ncbi.nlm.nih.gov/18084904/