Cold-inducible RNA-binding protein (CIRP) in inflammatory diseases: Molecular insights of its associated signalling pathways

Cold-inducible RNA-binding protein (CIRP) was previously identified as an intracellular stress-response protein, which can respond to a variety of stress conditions by changing its expression and regulating mRNA stability through its binding site on the 3 '-UTR of its targeted mRNAs. Recently, extracellular CIRP (eCIRP) was discovered to be present in various inflammatory conditions and could act as a pro-inflammatory factor. Genetic studies have demonstrated a key role for eCIRP in inflammatory conditions that led to the importance of targeting eCIRP in these diseases. Currently, the underlying mechanism of eCIRP-induced inflammation is under intensive investigation and several signalling pathways are being explored. Here, we epitomized various signalling pathways that mediate the pro-inflammatory effects of CIRP and also recapitulated all the CIRP-derived peptides that can block the interaction between CIRP and its receptors in inflammatory setting.

Automated summary

CIRP is a crucial stress-response protein that can adapt to various stress conditions intracellularly and act as a pro-inflammatory factor extracellularly in inflammatory settings. Genetic studies have highlighted the key role of eCIRP in inflammatory diseases, emphasizing the importance of targeting eCIRP in these conditions.