Endogenous inflammatory molecules engage Toll-like receptors in cardiovascular disease.
Innate immunity is important in the pathogenesis and progression of cardiovascular disease. Innate immune cells express various pattern-recognition receptors, among which also Toll-like receptors (TLRs). TLRs occur in atherosclerotic lesions where they are triggered by both exogenous (bacterial and viral pathogens) and endogenous (tissue damage-associated) molecules. Several endogenous TLR activators are described in relation to atherosclerotic disease or ischemia-induced cardiac injury. Experimental animal models have proved the role of TLR endogenous activators in disease initiation and further development. Nowadays, researchers aim to unravel the exact mechanisms involved in the endogenous ligand-dependent TLR signaling and to discover new potential activators, released during pathological conditions such as atherosclerosis and related ischemic manifestations. This review provides an overview of the currently known endogenous molecules which trigger innate immunity via TLRs in cardiovascular disease.
Ionita
Mihaela G
MG
Experimental Cardiology Laboratory, Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Arslan
Fatih
F
de Kleijn
Dominique P V
DP
Pasterkamp
Gerard
G
D000818:Animals; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000276:immunology*; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism*; D008024:Ligands; D051379:Mice; D051193:Toll-Like Receptors / Q000378:metabolism*
D002135:Calcium-Binding Proteins; D006360:Heat-Shock Proteins; D008024:Ligands; D051193:Toll-Like Receptors