Heat Shock Proteins in Tendinopathy: Novel Molecular Regulators

Figure 1

The biology of heat shock proteins in inflammatory disease. Tissue damage/stress results in the release of alarmins which in turn signal via the highlighted receptor complexes. HMGB1 and IL-33 also have intracellular nuclear functions when upregulated. This results in the release of further cytokines, growth factors, and changes in extracellular matrix production within the damaged tissue with pathological changes.