Review Article

The Entry and Egress of Monocytes in Atherosclerosis: A Biochemical and Biomechanical Driven Process

Table 2

Potential therapeutic approaches targeting plaque macrophages.

TargetMethod/drugsPossible mechanismsReferences

CCR2Nanoparticle-encapsulated siRNAReducing Lys6Chigh monocytes at the inflammation site and the inhibition of migration of bone marrow granulocyte macrophage progenitors into the blood[145, 146]
Monoclonal antibodies: MLN-1202Reducing serum C-reactive protein and preventing egress of CCR2-sensitive monocytes from the bone marrow[147]
AntagonistPropagermaniumSelectively inhibiting CCR2-mediated monocytes migration without affecting CCL2/CCR2 binding or CCL2-stimulated Ca2+ mobilization[148, 149]
TLK-19705A smaller but similar molecule like propagermanium[149]
GSK1344386BSelective CCR2 inhibition[150]
PA508CCL2 mutant as a CCL2 competitor, combine with CCR2 without functionally activation[151]

CCL2AntibodiesInhibiting macrophage infiltration while bringing some potential side effects such as neovascularization disorders and impaired immune system function[152]

CCR7Statins or bone marrow transplantationUpregulating CCR7, promoting the egress of macrophages from the plaque, and helping it return to the lymphoid tissue[154, 155]