Mannan-Binding Lectin in Cardiovascular Disease

Abstract

Cardiovascular disease remains the leading cause of mortality and morbidity worldwide so research continues into underlying mechanisms. Since innate immunity and its potent component mannan-binding lectin have been proven to play an important role in the inflammatory response during infection and ischaemia-reperfusion injury, attention has been paid to its role in the development of cardiovascular complications as well. This review provides a general outline of the structure and genetic polymorphism of MBL and its role in inflammation/tissue injury with emphasis on associations with cardiovascular disease. MBL appears to be involved in the pathogenesis of atherosclerosis and, in consequence, coronary artery disease and also inflammation and tissue injury after myocardial infarction and heart transplantation. The relationship between MBL and disease is rather complex and depends on different genetic and environmental factors. That could be why the data obtained from animal and clinical studies are sometimes contradictory proving not for the first time that innate immunity is a “double-edge sword,” sometimes beneficial and, at other times disastrous for the host.

Biological role of mannose binding lectin: From newborns to centenarians

“…More recent evidences in humans confirmed the beneficial effects of MBL deficiency in ischemic diseases: the reduced mortality for acute myocardial infarction reported in patients with MBL deficiency undergoing percutaneous coronary intervention; the long-lasting protection toward cerebral ischemia after the inhibition of MBL; the higher levels of MBL found in patients with unstable angina; and finally, the fatal outcome in an MBL deficient patient with myocardial infarction after MBL transfusion [31].…”

“…Myocardial reperfusion after ischemia triggers an inflammatory response that paradoxically counteracts the beneficial effects of the improved blood flow [31] and recruits either inflammatory or innate immunity mediators. Subsequently, studies in the mice model confirmed the disadvantageous effects of high biological activity of MBL in myocardial ischemic diseases, e.g., a high deposition of the protein in ischemic hearth, and the advantages of reduced MBL activity, e.g., the protection by cardiac damage and the reduction of the infarct area in MBL deficient mice [32].…”

Activation of the lectin pathway of complement by cardiopulmonary bypass contributes to the development of systemic inflammatory response syndrome after paediatric cardiac surgery

“…The complement system may be a key mechanism in the host response to CPB, and that could include the lectin pathway. Its potent activator, mannose‐binding lectin, plays an important role in the development of cardiovascular disease and ischaemia–reperfusion injury . Lectin pathway involvement in the reaction to CPB during adult cardiac surgery was reported originally by Hoedemaekers et al .…”

Distinct Longitudinal Associations of MBL, MASP-1, MASP-2, MASP-3, and MAp44 With Endothelial Dysfunction and Intima–Media Thickness

“…At baseline, 28% of the Cohort on Diabetes and Atherosclerosis Maastricht (CODAM) participants had CVD and 16% had CVE. In Table I 1,4,7,10 For this reason, the A/0 and 0/0 individuals were combined into 1 group in the regression analyses.…”

“…1 Several large studies that investigated mannose-binding lectin (MBL) in relation to the risk of CVD have yielded contradictory findings. Studies that investigated MBL genotypes as proxies for circulating MBL consistently found that genotypes that result in low or deficient MBL were a risk factor for the development of CVD.…”