Table 3.

Involvement of large middle molecules with cardiovascular disease

Middle MoleculeAssociationPossible Mechanisms
IL-18Cardiovascular mortality; aortic pulse wave velocity; unstable coronary plaque; coronary and thoracic aortic calcificationPromotion of atherosclerotic plaque instability, induction of IFN-γ, promotion of collagen and lipid deposition
IL-6Left ventricular hypertrophy, systolic dysfunction; cardiovascular mortalityCoordination of local inflammatory cell influx and lymphocyte proliferation; promotion of coagulation
IL-1βLeft ventricular hypertrophyPromotion of local inflammatory response within plaque
TNF-αLeft ventricular hypertrophyPromotion of cardiac inflammatory response to stress
Pentraxin-3Unstable coronary plaqueInfiltration of neutrophils into atherosclerotic plaque, prothrombotic effects, impairment of NO production
β-Trace proteinAtherosclerotic plaque; cardiovascular mortalityPossible functions acting against platelet aggregation via catalyzation of PGD2 production
ProlactinCardiovascular mortalityProliferation of vascular smooth muscle cells, promotion of vasoconstriction
AGEsCardiovascular mortalityDeposition within vessel wall; induction of oxidative stress, inflammation, and endothelial dysfunction
VisfatinUnstable atherosclerotic plaqueInduction of inflammatory macrophages within atherosclerotic plaque
AdiponectinAtherosclerotic plaqueExpression of adhesion molecules; foam cell formation
LeptinAtherosclerotic plaqueExpression of adhesion molecules; production of MCP-1, IL-6, and TNF-α
FGF-2Cardiac hypertrophyInduction of cardiomyocyte hypertrophic response
FGF-23Cardiac hypertrophyInduction of cardiomyocyte hypertrophic response
  • NO, nitric oxide; AGE, advanced glycosylation end products FGF, fibroblast growth factor.