Identification and functional exploration of Ferroptosis and Immune Related Long Non-Coding RNA in Inflammatory bowel disease

Hu, Yunhong; Sun, Shaopeng; Li, Heng

doi:10.21203/rs.3.rs-1857506/v1

Cited by 1 publication

(2 citation statements)

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“…In a similar study, the analysis of 97 Uc and 75 cd samples alongside 22 normal controls revealed six differently expressed long non-coding RNAs (lncRNAs) associated with ferroptosis and immunity in IBd. A constructed lncRNA-mRNA regulatory network further identified potential miRNAs and transcription factors based on trans and competing endogenous RNA mechanisms, concluding that ferroptosis and immune-related lncRNA are involved in the regulation of aberrant immune response in IBd (59). The implication of ferroptosis in IBd pathology, as outlined above, is illustrated in Fig.…”

Section: Role Of Ferroptosis In the Pathogenesis Of Ibdmentioning

confidence: 87%

“…Studies have indicated that the fundamental characteristics of ferroptosis, including increased lipid peroxidation, the depletion of GSH, the inactivation of GPX4 and elevated iron deposition, are manifested in the inflamed intestinal tissue of patients with IBd and in animal models of IBd (19,58,59). Ferroptosis is involved in IBd, particularly intestinal epithelial cell death (5).…”

Section: Role Of Ferroptosis In the Pathogenesis Of Ibdmentioning

confidence: 99%

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Role of ferroptosis in the pathogenesis and as a therapeutic target of inflammatory bowel disease (Review)

et al. 2023

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Ferroptosis, a novel form of regulated cell death, is characterized by the accumulation of labile iron and lipid peroxidation, and the excessive production of reactive oxygen species (ROS). Although ferroptosis lies at the center of crucial biological activities involving O 2 , iron and polyunsaturated fatty acids (PUFAs), which are essential for cell proliferation and growth, the interaction between these molecules could also mediate the accumulation of toxic levels of ROS and lipid peroxides, which can then cause damage to cellular membranes and ultimately result in cell death. Recent reports have indicated that ferroptosis participates in the development and progression of inflammatory bowel disease (IBD), offering a new exploratory field which may aid in the more in-depth understanding of the pathogenesis and therapeutic targets of IBd. Of note, the mitigation of the characteristic features of ferroptosis, such as depleted glutathione (GSH) levels, inactivated glutathione peroxidase 4 (GPX4), elevated levels of lipid peroxidation and iron overload significantly relieve IBD. This has attracted the attention of researches aiming to examine therapeutic agents that inhibit ferroptosis in IBd, including radical-trapping antioxidants, enzyme inhibitors, iron chelators, protein degradation inhibitors, stem cell-derived exosomes and oral N-acetylcysteine or glutathione. The present review summarizes and discusses the current data that implicate ferroptosis in the pathogenesis of IBd and its inhibition as a novel alternate therapeutic target for IBd. The mechanisms and key mediators of ferroptosis, including GSH/GPX4, PUFAs, iron and organic peroxides are also discussed. Although the field is relatively new, the therapeutic regulation of ferroptosis has exhibited promising outcomes as a novel treatment avenue for IBd. Contents 1. Introduction 2. The mechanisms of ferroptosis 3. Key mediators of ferroptosis 4. Role of ferroptosis in the pathogenesis of IBd 5. Role of ferroptosis in the pathogenesis of other intestinal diseases 6. Targeting ferroptosis for the treatment of IBd 7. Targeting ferroptosis in other intestinal diseases 8. conclusions and future perspectives

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Section: Role Of Ferroptosis In the Pathogenesis Of Ibdmentioning

confidence: 87%