Toll-Like Receptors in Ischaemia and Its Potential Role in the Pathophysiology of Muscle Damage in Critical Limb Ischaemia

Abstract EN

Toll-like receptors (TLRs) are key receptors of the innate immune system which are expressed on immune and nonimmune cells.

They are activated by both pathogen-associated molecular patterns and endogenous ligands.

Activation of TLRs culminates in the release of proinflammatory cytokines, chemokines, and apoptosis.

Ischaemia and ischaemia/reperfusion (I/R) injury are associated with significant inflammation and tissue damage.

There is emerging evidence to suggest that TLRs are involved in mediating ischaemia-induced damage in several organs.

Critical limb ischaemia (CLI) is the most severe form of peripheral arterial disease (PAD) and is associated with skeletal muscle damage and tissue loss; however its pathophysiology is poorly understood.

This paper will underline the evidence implicating TLRs in the pathophysiology of cerebral, renal, hepatic, myocardial, and skeletal muscle ischaemia and I/R injury and discuss preliminary data that alludes to the potential role of TLRs in the pathophysiology of skeletal muscle damage in CLI.