The dynamics of monocytes in the process of collateralization

Abstract

The present treatment for coronary artery disease mainly includes medication and drug therapy combined with coronary revascularization. However, the rate of restenosis after stent implantation is still as high as 10% to 20%, 1 and approximately 20% of patients with coronary artery diffuse multivessel disease are unable to tolerate percutaneous coronary intervention or coronary artery bypass grafting. 2 Then, does any strategy effectively alleviate myocardial ischemic symptoms for those patients? Collateral circulation might be the answer.Many clinical studies show that well-established collateral circulation can effectively protect cardiac muscle from ischemia and improve patients' prognoses. 3 Collateral vessel refers to the tiny anatomical microvessels that bridge the severe stenosis or occlusion between the proximal and distant parts of the same blood vessel or between different blood vessels, with a diameter of 20-350 μm, which can provide blood supply to the ischemic regions and confine myocardial infarct size. 4 Related studies have shown that good collateral circulation plays a role in protecting myocardium from acute myocardial infarction and chronic myocardial ischemia. 5-8 A metaanalysis enrolling 6529 participants from several studies showed that patients with high collateralization had a 36% reduction in death risk compared with patients with low collateralization. 9 Therefore, the establishment of coronary collateral circulation is of great significance for the prognosis of coronary artery disease.The development of collateral circulation refers to the remodeling and enlargement of pre-existing collateral vessels. 10 It is currently believed that when the coronary artery is stenotic or occluded, AbstractCollateralization is an important way for patients with coronary heart disease to supply blood flow to the ischemic area. At present, research on the mechanism of collateral circulation mainly focuses on the inflammatory response. Monocytes are the kernel of inflammatory response during arteriogenesis. Therefore, we reviewed the recent developments in this field in terms of the dynamic changes of monocytes during collateralization. We searched and scanned PubMed for the following terms until November 2018: collateral, collateralization, monocyte, macrophage, and arteriogenesis.Articles were obtained and examined to figure out the dynamics of monocytes in the progress of collateralization. Substantial research shows that recruitment, infiltration, and phenotypic transformation of monocytes can affect function in various ways, respectively. Mechanical or chemical factors that can produce effects on collateral development may be due partly to impact on dynamics of monocytes. Although mechanisms of dynamics of monocytes during arteriogenesis are not elucidated clearly, there is no doubt that deeper exploration of the underlying mechanisms will contribute to pharmaceutical development aiming for promoting collateral development. K E Y W O R D Sarteriogenesis, collateral, collateralization, macrophage, mono...

p38 MAPK priming boosts VSMC proliferation and arteriogenesis by promoting PGC1α-dependent mitochondrial dynamics

“…In addition, the generation of a new conditional mouse line has also allowed us to demonstrate the cell autonomous role of MT4-MMP in VSMC proliferation and arteriogenesis in vivo. Although Sm22 expression has been reported in peritoneal macrophages and blood neutrophils and monocytes 69 , cell lineages with potential beneficial actions in arteriogenesis 12 , 70 , we did observe the proliferative phenotype in MT4-MMP −/− VSMCs cultured in vitro, arguing in favour of a cell autonomous action.…”

Exercise Prior to Lower Extremity Peripheral Artery Disease Improves Endurance Capacity and Hindlimb Blood Flow by Inhibiting Muscle Inflammation

“…In the present study, we did not observe any impact of preventive exercise on ischemic muscle M2 macrophage gene expression at either 1 or 5 week post-PAD. The lack of changes in M2 macrophage phenotype might explain why VEGFA gene expression in ischemic muscle was not modulated with preventive exercise, since M2 macrophages are a major source of VEGF production ( 11 ). In agreement with our study, a reduction in M1 macrophages without affecting M2 macrophages has been also observed in gastrocnemius muscle from an animal model of Duchenne muscular dystrophy after 4 weeks of low intensity training ( 38 ).…”

“…Macrophages first infiltrating the ischemic muscle are polarized to the pro-inflammatory M1 (classically activated) phenotype (11,12). After predominantly early infiltration of M1 macrophages, a shift toward the anti-inflammatory M2 (alternatively activated) phenotype appears in later stage postischemia, promoting collateral growth and enhance blood flow recovery (11,12). Therefore, therapeutic interventions aiming at modulating the phenotype of macrophages in the ischemic muscle has been proved to be effective in improving perfusion in experimental PAD (13)(14)(15)(16)(17).…”

“…Macrophages undergo phenotype change according to specific environmental cues. Macrophages first infiltrating the ischemic muscle are polarized to the pro-inflammatory M1 (classically activated) phenotype ( 11 , 12 ). After predominantly early infiltration of M1 macrophages, a shift toward the anti-inflammatory M2 (alternatively activated) phenotype appears in later stage post-ischemia, promoting collateral growth and enhance blood flow recovery ( 11 , 12 ).…”

Correlation of plasma vitamin D levels with coronary collateral circulation

“…However, the exact physiologic and pathologic mechanisms affecting the development of CCC have not yet been known. Several studies reported the vascular endothelial cells have fundamental roles in the maturation of coronary collaterals (17,18). It seems that vitamin D deficiency plays a pivotal role in CCC development via abnormalities in leukocyte adhesion, proliferation of vascular smooth muscle cells and vascular endothelial development factor (19).…”