Heat Shock Protein Modulation in Inflammatory Bowel Diseases

Heat shock proteins (HSPs) are evolutionarily conserved molecular chaperones that maintain proteome integrity and regulate cellular stress responses. In the context of inflammatory bowel diseases (IBD), which encompass Crohn’s disease and ulcerative colitis, HSPs contribute to epithelial barrier protection, immune‐cell homeostasis and resolution of inflammation. Dysregulation of HSP expression has been linked to breakdown of tight junctions, excessive cytokine release and aberrant activation of innate sensors such as the inflammasome. Conversely, targeted induction or exogenous delivery of specific HSPs can restore mucosal integrity, skew macrophages towards anti‐inflammatory phenotypes and suppress oxidative stress. Modulation of HSP activity—either through small‐molecule inhibitors or recombinant chaperones—offers promising avenues for novel diagnostics and therapies. Recent advances also highlight the dual nature of the heat shock response, whereby certain family members may foster fibrotic remodelling or neoplastic progression if chronically overexpressed. Understanding the balance between protective and pathogenic roles of HSPs is essential for optimising interventions in IBD.

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Heat Shock Protein Modulation in Inflammatory Bowel Diseases publication trend

The graph below shows the total number of articles in heat shock protein modulation in inflammatory bowel diseases across all publications each year (not limited to Nature Index journals).

Technical terms

Heat shock proteins (HSPs): Molecular chaperones that ensure correct protein folding and cellular homeostasis under stress conditions.

Inflammasome: A multiprotein complex that activates inflammatory caspases and cytokine maturation in response to cellular stress.

Mitophagy: Selective autophagic removal of damaged mitochondria to maintain cellular energy balance and limit reactive oxygen species.

Macrophage polarization: Functional differentiation of macrophages into pro-inflammatory (M1) or anti-inflammatory (M2) phenotypes.

Toll-like receptor 4 (TLR4): A pattern recognition receptor that senses microbial components and initiates inflammatory signalling cascades.

NF-κB: A transcription factor central to the regulation of genes controlling immune and inflammatory responses.

References

1. Secreted glucose regulated protein78 ameliorates DSS-induced mouse colitis. Frontiers in Immunology (2023).
2. Inflammatory Bowel Diseases: An Updated Overview on the Heat Shock Protein Involvement. International Journal of Molecular Sciences (2023).
3. The Functions and Therapeutic Potential of Heat Shock Proteins in Inflammatory Bowel Disease—An Update. International Journal of Molecular Sciences (2019).
4. Heat Shock Transcription Factor 2 Promotes Mitophagy of Intestinal Epithelial Cells Through PARL/PINK1/Parkin Pathway in Ulcerative Colitis. Frontiers in Pharmacology (2022).