The mechanisms that modulate the response to tissue injury are not fully understood. Abnormalities
in the repair response are associated with a variety of chronic disease states characterized
by inflammation, followed subsequently by excessive ECM deposition. As cell-matrix interactions are
able to regulate cellular homeostasis, modification of ECM integrity appears to be an unspecific factor
in promoting the onset and progression of inflammatory diseases. Evidence is emerging to show that
endogenous ECM molecules supply signals to damage tissues and cells in order to promote further
ECM degradation and inflammation progression. Several investigations have been confirmed that HA
fragments of different molecular sizes exhibit different biological effects and responses. In fact, the increased
deposition of HA into the ECM is a strong hallmark of inflammation processes. In the context
of inflammatory pathologies, highly polymerized HA is broken down into small components, which
are able to exacerbate the inflammatory response by inducing the release of various detrimental mediators
such as reactive oxygen species, cytokines, chemokines and destructive enzymes and by facilitating
the recruitment of leukocytes. However, strategies involving the modulation of the HA fragment
with specific receptors on cell surface could represent different promising effects for therapeutic scope.
This review will focus on the inflammation action of small HA fragments in recent years obtained by
in vivo reports.