Integrated Multi-Omics Analysis Reveals the Mechanisms of Intestinal Cell Injury Under Different Levels of Heat Stress
文献类型: 外文期刊
作者: Feng, Yuchao 1 ; Suo, Decheng 1 ; Gong, Ping 3 ; Wei, Peiling 3 ; Zhang, Lu 4 ; Zhang, Shu 2 ; Li, Xiaonan 1 ; Wang, Changyuan 2 ; Fan, Xia 1 ;
作者机构: 1.Chinese Acad Agr Sci, Inst Qual Stand & Testing Technol Agroprod, State Key Lab Qual & Safety Agroprod, Beijing 100081, Peoples R China
2.Heilongjiang Bayi Agr Univ, Coll Food, Daqing 163319, Peoples R China
3.Xinjiang Acad Anim Sci, Inst Anim Husb Qual Stand, Urumqi 830057, Peoples R China
4.Ctr Agroprod Safety & Qual Xinjiang, Urumqi 830006, Peoples R China
关键词: heat stress; metabolomics; transcriptomics; mechanisms; pathway
期刊名称:INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES ( 影响因子:4.9; 五年影响因子:5.7 )
ISSN: 1661-6596
年卷期: 2025 年 26 卷 12 期
页码:
收录情况: SCI
摘要: Given the escalating global temperatures and the consequent exacerbation of heat stress, dietary interventions have emerged as a promising therapeutic strategy. The gastrointestinal tract, being exquisitely sensitive to thermal challenges, revealing the underlying mechanisms of intestinal cell injury under high temperature, is essential for developing strategies to prevent heat stress. Here, we integrated metabolomic and transcriptomic analyses to investigate the metabolic and genetic changes in murine intestinal cells in response to different levels of heat stress. The results identified the PI3k-Akt-FoxO pathway as the major heat stress regulatory pathway Kin MODE-K cells. The possible regulatory mechanism is to reduce the expression of the FoxO gene through the downstream phosphorylation of PI3K under the stimulation of growth factors such as INS, IGF1 and TGF-beta. Then, through acetylation modification, it regulates the expression of the Gadd45 gene, promotes the expression of p19 and BNIP3 genes, and inhibits the expression of the ATG8 gene, thus inducing apoptosis to remove cells that cannot be repaired. It also promotes cyclinB, PLK, and Bcl-6 gene expression in cells surrounding apoptotic cells to inhibit apoptosis. It promotes the expression of RAG1/2 to enhance cellular immunity and regulates the G6pc gene to maintain the homeostasis of glycogen metabolism and glucose under heat stress. Our findings provide a basis for the regulation of intestinal cell damage due to heat stress through dietary interventions.
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