TY - JOUR
T1 - CD40-CD40L interactions in atherosclerosis
AU - Lutgens, Esther
AU - Daemen, Mat J.A.P.
N1 - Funding Information:
This research has been supported by a grant from the Dutch Heart Foundation. E.L. is a postdoctoral fellow of the Dr. E. Dekker program (D2000-41).
PY - 2002
Y1 - 2002
N2 - Increasing evidence supports a central role for CD40-CD40L interactions in the pathogenesis of atherosclerosis. Recently, we have shown that CD40L deficiency as well as pharmacological inhibition of CD40L in ApoE-/- mice results in the development of a stable atherosclerotic plaque phenotype. This phenotype is rich in smooth muscle cells and collagen, and contains only a small amount of macrophages and T-lymphocytes. CD40 and CD40L protein are present in almost all cell types in human atherosclerotic lesions. Expression was observed in early plaques, but was more predominant in advanced, rupture-prone, and ruptured plaques. Because most of the acute complications of atherosclerosis are the result of plaque rupture, CD40L inhibition might be a novel therapeutic approach to prevent atherosclerotic plaque destabilization and plaque rupture.
AB - Increasing evidence supports a central role for CD40-CD40L interactions in the pathogenesis of atherosclerosis. Recently, we have shown that CD40L deficiency as well as pharmacological inhibition of CD40L in ApoE-/- mice results in the development of a stable atherosclerotic plaque phenotype. This phenotype is rich in smooth muscle cells and collagen, and contains only a small amount of macrophages and T-lymphocytes. CD40 and CD40L protein are present in almost all cell types in human atherosclerotic lesions. Expression was observed in early plaques, but was more predominant in advanced, rupture-prone, and ruptured plaques. Because most of the acute complications of atherosclerosis are the result of plaque rupture, CD40L inhibition might be a novel therapeutic approach to prevent atherosclerotic plaque destabilization and plaque rupture.
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U2 - 10.1016/S1050-1738(01)00142-6
DO - 10.1016/S1050-1738(01)00142-6
M3 - Review article
C2 - 11796241
AN - SCOPUS:0036140664
SN - 1050-1738
VL - 12
SP - 27
EP - 32
JO - Trends in cardiovascular medicine
JF - Trends in cardiovascular medicine
IS - 1
ER -