The STING-IRF3 pathway contributes to paraquat-induced acute lung injury

Interferon Regulatory Factors (IRFs), a family of transcription factors, profoundly influence the immune system, impacting both physiological and pathological processes. This review explores the diverse functions of nine mammalian IRF members, each featuring conserved domains essential for interactions with other transcription factors and cofactors. These interactions allow IRFs to modulate a broad spectrum of physiological processes, encompassing host defense, immune response, and cell development. Conversely, their pivotal role in immune regulation implicates them in the pathophysiology of various diseases, such as infectious diseases, autoimmune disorders, metabolic diseases, and cancers. In this context, IRFs display a dichotomous nature, functioning as both tumor suppressors and promoters, contingent upon the specific disease milieu. Post-translational modifications of IRFs, including phosphorylation and ubiquitination, play a crucial role in modulating their function, stability, and activation. As prospective biomarkers and therapeutic targets, IRFs present promising opportunities for disease intervention. Further research is needed to elucidate the precise mechanisms governing IRF regulation, potentially pioneering innovative therapeutic strategies, particularly in cancer treatment, where the equilibrium of IRF activities is of paramount importance.

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The STING-IRF3 pathway contributes to paraquat-induced acute lung injury

Cited by 4 publications

References 41 publications

Diallyl disulfide suppresses the lipopolysaccharide-driven inflammatory response of macrophages by activating the Nrf2 pathway

Diallyl disulfide suppresses the lipopolysaccharide-driven inflammatory response of macrophages by activating the Nrf2 pathway

Signaling pathways involved in paraquat-induced pulmonary toxicity: Molecular mechanisms and potential therapeutic drugs

The multiple roles of interferon regulatory factor family in health and disease

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