Cellular and Pharmacological Targets to Induce Coronary Arteriogenesis

Hollander, Maurits R.; Horrevoets, Anton J.G.; Royen, Niels van

doi:10.2174/1573403x113099990003

Cited by 15 publications

(29 citation statements)

References 87 publications

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“…In VEGF signaling, there are three primary cell-surface receptors to which it binds: two tyrosine kinase receptors VEGFR-1 and VEGFR-2 and a nonkinase receptor neuropilin-1 (NRP-1) [35][36][37]. There are multiple isoforms of VEGF, with VEGF-A playing the major role in endothelial cell function via binding to .…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

“…In addition to endothelial cells, macrophages are also heavily involved in arteriogenesis, but in order to do so must be directed to the correct location [36]. The primary molecule that has been studied as part of this mechanism is monocyte chemotactic protein 1 (MCP-1) [36].…”

Section: Mcp-1 and Macrophagesmentioning

confidence: 99%

“…Under hypoxic conditions, VEGF production and release stimulates new capillary formation (angiogenesis) via endothelial cell sprouting, proliferation, and migration [35]. Alternatively, under diferent conditions, it can instead stimulate growth of new arteries, formation of collateral vessels, and modulation of lumen expansion-these actions are collectively referred to as arteriogenesis [35].In VEGF signaling, there are three primary cell-surface receptors to which it binds: two tyrosine kinase receptors VEGFR-1 and VEGFR-2 and a nonkinase receptor neuropilin-1 (NRP-1) [35][36][37]. There are multiple isoforms of VEGF, with VEGF-A playing the major role in endothelial cell function via binding to .…”

mentioning

confidence: 99%

“…In the last step of the cycle, release of inlammatory cytokines by recruited monocytes cause increased secretion of MCP-1 from the endothelium, resulting in further monocyte recruitment [45]. Of similarly signiicant importance to MCP-1 are two adhesive molecules, intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), which serve to bind the surface of migrating monocytes allowing them to roll along the luminal surface of the vasculature [36].Once the macrophages have reached their destination, the correct phenotype must be expressed to stimulate new vessel growth [36]. There are two primary phenotypes of monocyte macrophages: M1 macrophages that secrete inlammatory molecules and help ight pathogens and M2…”

mentioning

confidence: 99%

“…Of similarly signiicant importance to MCP-1 are two adhesive molecules, intracellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), which serve to bind the surface of migrating monocytes allowing them to roll along the luminal surface of the vasculature [36].…”

mentioning

confidence: 99%

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Coronary Collateral Growth: Clinical Perspectives and Recent Insights

Patel¹,

Hopmann²,

Desai³

et al. 2017

Physiologic and Pathologic Angiogenesis - Signaling Mechanisms and Targeted Therapy

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This chapter summarizes recent research on the coronary collateral circulation. The chapter is focused on clinical perspectives and importance of a well-developed coronary collateral circulation, the mechanisms of growth induced by chemical factors and a role for stem cells in the process. Some discussion is devoted to the role of shear stress and mechanical signaling, but because this topic has been reviewed so extensively in the recent past, there is only small mention of its role in the growth of the coronary collateral circulation.Keywords: arteriogenesis, coronary collateral, ischemic heart disease IntroductionAlthough arteriogenesis has been studied for approximately a hundred years, there are still fundamental unanswered questions about the causes of collateral vessel growth, and whether diferent factors control growth at varying points in the maturation process. One line of investigation, spurred by the myriad contributions of Schaper and his colleagues have focused on mechanical shear stress being the main factor that stimulates collateral growth [1][2][3][4]. Although this hypothesis is well-founded on a large body of experimental data, it does not explain other observations that show collateral growth in the absence of altered shear stress [5,6]. Accordingly investigators have proposed that ischemia (via cytokine, chemokine, and growth factor expression), and the consequential inlammation, is the cause of collateral growth, but © 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.assessing it has proven to be diicult due to the unclear lines between ischemic regions, normal circulation, and collateral growth. The hypotheses regarding the causative factor(s) for collateral growth are not mutually exclusive as there are likely many mechanisms that are the principal driver, which vary at various points of the process. For example, even if one maintains that ischemia is the initiating mechanism for collateral growth, it is likely that other stimuli continue the growth of the vessel after the ischemic stimulus has waned. To provide perspective for this chapter, we refer to Figure 1, which summarizes four factors that exert important efects in this adaptive process. The bulk of this chapter will focus on the collateral growth from a clinical perspective, the role of stem cells, and chemical factors involved in this process. We will not extensively review the role that shear stress in coronary collateral growth as this has been reviewed ample times in the past. We also will not review the genetic aspects because the bulk of this information has been derived from studies of collateral growth in vascular beds other than the heart, e.g., skeletal muscle and brain [7,8], although there is some preliminary information about genetic links to collateral growth in patie...

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Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

Section: Mcp-1 and Macrophagesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Coronary Collateral Growth: Clinical Perspectives and Recent Insights

Patel¹,

Hopmann²,

Desai³

et al. 2017

Physiologic and Pathologic Angiogenesis - Signaling Mechanisms and Targeted Therapy

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Biomechanics in Small Artery Remodeling

Bakker

VanBavel

2021

Vascular Mechanobiology in Physiology and Disease

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CD40 in coronary artery disease: a matter of macrophages?

et al. 2016

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Coronary artery disease (CAD), also known as ischemic heart disease (IHD), is the leading cause of mortality in the western world, with developing countries showing a similar trend. With the increased understanding of the role of the immune system and inflammation in coronary artery disease, it was shown that macrophages play a major role in this disease. Costimulatory molecules are important regulators of inflammation, and especially, the CD40L-CD40 axis is of importance in the pathogenesis of cardiovascular disease. Although it was shown that CD40 can mediate macrophage function, its exact role in macrophage biology has not gained much attention in cardiovascular disease. Therefore, the goal of this review is to give an overview on the role of macrophage-specific CD40 in cardiovascular disease, with a focus on coronary artery disease. We will discuss the function of CD40 on the macrophage and its (proposed) role in the reduction of atherosclerosis, the reduction of neointima formation, and the stimulation of arteriogenesis.

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Cellular and Pharmacological Targets to Induce Coronary Arteriogenesis

Cited by 15 publications

References 87 publications

Coronary Collateral Growth: Clinical Perspectives and Recent Insights

Coronary Collateral Growth: Clinical Perspectives and Recent Insights

Biomechanics in Small Artery Remodeling

CD40 in coronary artery disease: a matter of macrophages?

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