Disclosures: Binu John: Exact Sciences: Grant/Research Support, Genentech: Grant/Research Support, Glycotest, Inc: Grant/Research Support, Gilead: Grant/Research Support, Exelixis: Consultant, Takeda: Grant/Research Support, GlaxoSmithKline: Consultant, Astra Zeneca: Consultant, Yangyang Deng: Nothing to Disclose, Amit Singal: Genentech: Consultant, AstraZeneca: Consultant, Bayer: Consultant, Eisai: Consultant, Exelixis: Consultant, Merck: Consultant, Elevar: Consultant, FujiFilm Medical Sciences: Consultant, Exact Sciences: Consultant, Glycotest: Consultant, Boston Scientific: Consultant, Sirtex: Consultant, HistoSonics: Consultant, Bassam Dahman: Nothing to Disclose 1015 GUT MICROBE-PRODUCED INDOLE-3-PROPIONIC ACID ALLEVIATES HEPATITIS B-RELATED FIBROSIS BY REGULATING TH17 CELL DIFFERENTIATION THROUGH GLUCOSE METABOLISM REPROGRAMMING Fangyuan Chen 1 Siqi Wang 1 Linlin Zheng 1 Shuyu Li 1 Jian Wu 2 Wei Jiang 3 , 1 Fudan University, Zhongshan Hospital, 2 Fudan University, 3 Fudan Univertisy, Zhongshan Hospital Background: T helper (Th) 17 play a crucial role in promoting HSC activation in fibrotic progression by producing interleukin-17 (IL-17)
The resulting GO/ KEGG terms highlighted the major biological processes influenced by METTL3-induced m6A transcriptional modifications in MASLD, particularly the KEGG terms
The TSP is dependent on the action of CBS and CSE, which can also act in cysteine catabolism (Figure 1B)
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A plausible explanation of this apparent dichotomy is that p53 promotes cell survival by preventing excessive increases in ROS under moderate oxidative stress, whereas when the oxygen species increase over a threshold level, it switches to becoming a ROS inducer, triggering cell death
