Abstract
Despite significant progress in IBD treatment in recent years, some patients remain insensitive or non-responsive towards existing treatments. [...]exploring IBD pathogenesis to develop novel therapeutic drugs or drug combinations is quite necessary. [7] Transcription factors and ferroptosis in IBD: [...]several transcription factors, such as nuclear factor erythrocyte 2-related factor 2 (Nrf2), nuclear factor κB (NF-κB), and signal transducer and activator of transcription 3 (STAT3), coordinate susceptibility to ferroptosis through transcription-dependent or non-transcriptional mechanisms [Supplementary Figure 2, http://links.lww.com/CM9/B954]. [1] STAT3 is a crucial transcription factor involved in the response to oxidative stress, and its primary active form is phosphorylated STAT3, which plays a significant role in ferroptosis. Previous studies have demonstrated the significant regulatory role of gut microbial metabolites in cell death [Supplementary Table 2, http://links.lww.com/CM9/B954], including apoptosis, autophagy, pyroptosis, and necroptosis.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Department of Gastroenterology and Hepatology, Tianjin Medical University General Hospital, Tianjin Medical University, Tianjin 300070, China
2 Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Tianjin Medical University, Tianjin 300070, China