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Arteriogenesis and Therapeutic Neovascularization

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A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (30 November 2019) | Viewed by 53983

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Special Issue Editors

Prof. Dr. Elisabeth Deindl

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Guest Editor

Walter-Brendel-Centre of Experimental Medicine, University Hospital, Ludwig-Maximilians-Universität München, 81377 Munich, Germany
Interests: cardiovascular research; immunology
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Paul Quax

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1. Department of Surgery, Leiden University Medical Center, 2333 ZA Leiden, The Netherlands
2. Einthoven Laboratory for Experimental Vascular Medicine Leiden University Medical Center, 2333 ZA Leiden, The Netherlands
Interests: experimental vascular medicine; blood vessel; arteriogenesis
Special Issues, Collections and Topics in MDPI journals

Prof. Johannes Waltenberger

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Westfälische Wilhelms-Universität Münster, Münster, Germany
Interests: collateral growth; arteriogenesis; diabetic paradox in vascular medicine

Prof. Thomas Schmitz-Rixen

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Guest Editor

Goethe-University, Dep. of Vascular and Endovascular Surgery, Frankfurt am Main, Germany
Interests: arteriogenesis; aortic aneurysm

Special Issue Information

Dear Colleagues,

Arteriogenesis, also frequently called collateral formation or even therapeutic angiogenesis, comprises those processes that lead to the formation and growth of collateral blood vessels that can act as natural bypasses to restore blood flow to distal tissues in occluded arteries. Both in coronary occlusive artery diseases as well as in peripheral occlusive arterial disease, arteriogenesis may play an important role in the restoration of blood flow. Despite the big clinical potential and the many promising clinical trials on arteriogenesis and therapeutic angiogenesis, the exact molecular mechanisms involved in the multifactorial processes of arteriogenesis are still not completely understood. In this inflammatory-driven vascular remodeling process, many cell types, both vascular cells and immune cells, many cytokines and growth factors, as well as various noncoding RNAs or progenitor cells may be involved. Consequently, many questions regarding the exact molecular mechanisms involved in the regulation of the arteriogenic response still need to be answered, and these answers will contribute to defining new therapeutic options.

This Special Issue of Cells is devoted to all aspects of arteriogenesis and collateral formation. It will contain articles that collectively provide a balanced, state-of-the-art view on various aspects of arteriogenesis and the underlying regulation of vascular remodeling. We seek submissions of high-quality articles on all aspects of arteriogenesis, including but not limited to regulatory mechanisms, the cell types involved, state-of-the-art models, latest (pre)clinical developments, and therapeutic options.

Prof. Elisabeth Deindl
Prof. Paul H. Quax
Prof. Johannes Waltenberger
Prof. Thomas Schmitz-Rixen
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

arteriogenesis
natural bypass growth
vascular remodeling
neovascularization
innate immunity
shear stress
mechanotransduction
mechanosensing
cell signalling cascades
leukocytes

Published Papers (13 papers)

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Editorial

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3 pages, 168 KiB

Open AccessEditorial

Arteriogenesis and Therapeutic Angiogenesis in Its Multiple Aspects

by Elisabeth Deindl and Paul H. A. Quax

Cells 2020, 9(6), 1439; https://doi.org/10.3390/cells9061439 - 10 Jun 2020

Cited by 8 | Viewed by 2225

Abstract

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

Research

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11 pages, 5551 KiB

Open AccessArticle

Control of Angiogenesis via a VHL/miR-212/132 Axis

by Zhiyong Lei, Timothy D. Klasson, Maarten M. Brandt, Glenn van de Hoek, Ive Logister, Caroline Cheng, Pieter A. Doevendans, Joost P. G. Sluijter and Rachel H. Giles

Cells 2020, 9(4), 1017; https://doi.org/10.3390/cells9041017 - 19 Apr 2020

Cited by 11 | Viewed by 3746

Abstract

A common feature of tumorigenesis is the upregulation of angiogenesis pathways in order to supply nutrients via the blood for the growing tumor. Understanding how cells promote angiogenesis and how to control these processes pharmaceutically are of great clinical interest. Clear cell renal cell carcinoma (ccRCC) is the most common form of sporadic and inherited kidney cancer which is associated with excess neovascularization. ccRCC is highly associated with biallelic mutations in the von Hippel–Lindau (VHL) tumor suppressor gene. Although upregulation of the miR-212/132 family and disturbed VHL signaling have both been linked with angiogenesis, no evidence of a possible connection between the two has yet been made. We show that miRNA-212/132 levels are increased after loss of functional pVHL, the protein product of the VHL gene, in vivo and in vitro. Furthermore, we show that blocking miRNA-212/132 with anti-miRs can significantly alleviate the excessive vascular branching phenotype characteristic of vhl^−/− mutant zebrafish. Moreover, using human umbilical vascular endothelial cells (HUVECs) and an endothelial cell/pericyte coculture system, we observed that VHL knockdown promotes endothelial cells neovascularization capacity in vitro, an effect which can be inhibited by anti-miR-212/132 treatment. Taken together, our results demonstrate an important role for miRNA-212/132 in angiogenesis induced by loss of VHL. Intriguingly, this also presents a possibility for the pharmaceutical manipulation of angiogenesis by modulating levels of MiR212/132. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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14 pages, 3806 KiB

Open AccessArticle

The Lipopeptide MALP-2 Promotes Collateral Growth

by Kerstin Troidl, Christian Schubert, Ann-Kathrin Vlacil, Ramesh Chennupati, Sören Koch, Jutta Schütt, Raghav Oberoi, Wolfgang Schaper, Thomas Schmitz-Rixen, Bernhard Schieffer and Karsten Grote

Cells 2020, 9(4), 997; https://doi.org/10.3390/cells9040997 - 16 Apr 2020

Cited by 11 | Viewed by 4954

Abstract

Beyond their role in pathogen recognition and the initiation of immune defense, Toll-like receptors (TLRs) are known to be involved in various vascular processes in health and disease. We investigated the potential of the lipopeptide and TLR2/6 ligand macrophage activating protein of 2-kDA (MALP-2) to promote blood flow recovery in mice. Hypercholesterolemic apolipoprotein E (Apoe)-deficient mice were subjected to microsurgical ligation of the femoral artery. MALP-2 significantly improved blood flow recovery at early time points (three and seven days), as assessed by repeated laser speckle imaging, and increased the growth of pre-existing collateral arteries in the upper hind limb, along with intimal endothelial cell proliferation in the collateral wall and pericollateral macrophage accumulation. In addition, MALP-2 increased capillary density in the lower hind limb. MALP-2 enhanced endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) release from endothelial cells and improved the experimental vasorelaxation of mesenteric arteries ex vivo. In vitro, MALP-2 led to the up-regulated expression of major endothelial adhesion molecules as well as their leukocyte integrin receptors and consequently enhanced the endothelial adhesion of leukocytes. Using the experimental approach of femoral artery ligation (FAL), we achieved promising results with MALP-2 to promote peripheral blood flow recovery by collateral artery growth. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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15 pages, 5668 KiB

Open AccessFeature PaperArticle

Contribution of the Potassium Channels K_V1.3 and K_Ca3.1 to Smooth Muscle Cell Proliferation in Growing Collateral Arteries

by Manuel Lasch, Amelia Caballero Martinez, Konda Kumaraswami, Hellen Ishikawa-Ankerhold, Sarah Meister and Elisabeth Deindl

Cells 2020, 9(4), 913; https://doi.org/10.3390/cells9040913 - 08 Apr 2020

Cited by 11 | Viewed by 2960

Abstract

Collateral artery growth (arteriogenesis) involves the proliferation of vascular endothelial cells (ECs) and smooth muscle cells (SMCs). Whereas the proliferation of ECs is directly related to shear stress, the driving force for arteriogenesis, little is known about the mechanisms of SMC proliferation. Here we investigated the functional relevance of the potassium channels K_V1.3 and K_Ca3.1 for SMC proliferation in arteriogenesis. Employing a murine hindlimb model of arteriogenesis, we found that blocking K_V1.3 with PAP-1 or K_Ca3.1. with TRAM-34, both interfered with reperfusion recovery after femoral artery ligation as shown by Laser-Doppler Imaging. However, only treatment with PAP-1 resulted in a reduced SMC proliferation. qRT-PCR results revealed an impaired downregulation of α smooth muscle-actin (αSM-actin) and a repressed expression of fibroblast growth factor receptor 1 (Fgfr1) and platelet derived growth factor receptor b (Pdgfrb) in growing collaterals in vivo and in primary murine arterial SMCs in vitro under K_V1.3. blockade, but not when K_Ca3.1 was blocked. Moreover, treatment with PAP-1 impaired the mRNA expression of the cell cycle regulator early growth response-1 (Egr1) in vivo and in vitro. Together, these data indicate that K_V1.3 but not K_Ca3.1 contributes to SMC proliferation in arteriogenesis. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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13 pages, 4620 KiB

Open AccessArticle

Local Mast Cell Activation Promotes Neovascularization

by Ilze Bot, Daniël van der Velden, Merel Bouwman, Mara J. Kröner, Johan Kuiper, Paul H. A. Quax and Margreet R. de Vries

Cells 2020, 9(3), 701; https://doi.org/10.3390/cells9030701 - 12 Mar 2020

Cited by 17 | Viewed by 3271

Abstract

Mast cells have been associated with arteriogenesis and collateral formation. In advanced human atherosclerotic plaques, mast cells have been shown to colocalize with plaque neovessels, and mast cells have also been associated with tumor vascularization. Based on these associations, we hypothesize that mast cells promote angiogenesis during ischemia. In human ischemic muscle tissue from patients with end-stage peripheral artery disease, we observed activated mast cells, predominantly located around capillaries. Also, in mouse ischemic muscles, mast cells were detected during the revascularization process and interestingly, mast cell activation status was enhanced up to 10 days after ischemia induction. To determine whether mast cells contribute to both arteriogenesis and angiogenesis, mast cells were locally activated immediately upon hind limb ischemia in C57Bl/6 mice. At day 9, we observed a 3-fold increase in activated mast cell numbers in the inguinal lymph nodes. This was accompanied by an increase in the amount of Ly6C^high inflammatory monocytes. Interestingly, local mast cell activation increased blood flow through the hind limb (46% at day 9) compared to that in non-activated control mice. Histological analysis of the muscle tissue revealed that mast cell activation did not affect the number of collaterals, but increased the collateral diameter, as well as the number of CD31⁺ capillaries. Together, these data illustrate that locally activated mast cell contribute to arteriogenesis and angiogenesis. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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18 pages, 6255 KiB

Open AccessFeature PaperArticle

Prolonged Hyperoxygenation Treatment Improves Vein Graft Patency and Decreases Macrophage Content in Atherosclerotic Lesions in ApoE3*Leiden Mice

by Laura Parma, Hendrika A. B. Peters, Fabiana Baganha, Judith C. Sluimer, Margreet R. de Vries and Paul H.A. Quax

Cells 2020, 9(2), 336; https://doi.org/10.3390/cells9020336 - 01 Feb 2020

Cited by 9 | Viewed by 3006

Abstract

Unstable atherosclerotic plaques frequently show plaque angiogenesis which increases the chance of rupture and thrombus formation leading to infarctions. Hypoxia plays a role in angiogenesis and inflammation, two processes involved in the pathogenesis of atherosclerosis. We aim to study the effect of resolution of hypoxia using carbogen gas (95% O₂, 5% CO₂) on the remodeling of vein graft accelerated atherosclerotic lesions in ApoE3*Leiden mice which harbor plaque angiogenesis. Single treatment resulted in a drastic decrease of intraplaque hypoxia, without affecting plaque composition. Daily treatment for three weeks resulted in 34.5% increase in vein graft patency and increased lumen size. However, after three weeks intraplaque hypoxia was comparable to the controls, as were the number of neovessels and the degree of intraplaque hemorrhage. To our surprise we found that three weeks of treatment triggered ROS accumulation and subsequent Hif1a induction, paralleled with a reduction in the macrophage content, pointing to an increase in lesion stability. Similar to what we observed in vivo, in vitro induction of ROS in bone marrow derived macrophages lead to increased Hif1a expression and extensive DNA damage and apoptosis. Our study demonstrates that carbogen treatment did improve vein graft patency and plaque stability and reduced intraplaque macrophage accumulation via ROS mediated DNA damage and apoptosis but failed to have long term effects on hypoxia and intraplaque angiogenesis. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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17 pages, 3129 KiB

Open AccessArticle

Isoform-Specific Roles of ERK1 and ERK2 in Arteriogenesis

by Nicolas Ricard, Jiasheng Zhang, Zhen W. Zhuang and Michael Simons

Cells 2020, 9(1), 38; https://doi.org/10.3390/cells9010038 - 21 Dec 2019

Cited by 18 | Viewed by 3191

Abstract

Despite the clinical importance of arteriogenesis, this biological process is poorly understood. ERK1 and ERK2 are key components of a major intracellular signaling pathway activated by vascular endothelial growth (VEGF) and FGF2, growth factors critical to arteriogenesis. To investigate the specific role of each ERK isoform in arteriogenesis, we used mice with a global Erk1 knockout as well as Erk1 and Erk2 floxed mice to delete Erk1 or Erk2 in endothelial cells, macrophages, and smooth muscle cells. We found that ERK1 controls macrophage infiltration following an ischemic event. Loss of ERK1 in endothelial cells and macrophages induced an excessive macrophage infiltration leading to an increased but poorly functional arteriogenesis. Loss of ERK2 in endothelial cells leads to a decreased arteriogenesis due to decreased endothelial cell proliferation and a reduced eNOS expression. These findings show for the first time that isoform-specific roles of ERK1 and ERK2 in the control of arteriogenesis. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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17 pages, 2805 KiB

Open AccessArticle

VEGF-A-Cleavage by FSAP and Inhibition of Neo-Vascularization

by Özgür Uslu, Joerg Herold and Sandip M. Kanse

Cells 2019, 8(11), 1396; https://doi.org/10.3390/cells8111396 - 06 Nov 2019

Cited by 7 | Viewed by 3375

Abstract

Alternative splicing leads to the secretion of multiple forms of vascular endothelial growth factor-A (VEGF-A) that differ in their activity profiles with respect to neovascularization. FSAP (factor VII activating protease) is the zymogen form of a plasma protease that is activated (FSAPa) upon tissue injury via the release of histones. The purpose of the study was to determine if FSAPa regulates VEGF-A activity in vitro and in vivo. FSAP bound to VEGF₁₆₅, but not VEGF₁₂₁, and VEGF₁₆₅ was cleaved in its neuropilin/proteoglycan binding domain. VEGF₁₆₅ cleavage did not alter its binding to VEGF receptors but diminished its binding to neuropilin. The stimulatory effects of VEGF₁₆₅ on endothelial cell proliferation, migration, and signal transduction were not altered by FSAP. Similarly, proliferation of VEGF receptor-expressing BAF3 cells, in response to VEGF₁₆₅, was not modulated by FSAP. In the mouse matrigel model of angiogenesis, FSAP decreased the ability of VEGF₁₆₅, basic fibroblast growth factor (bFGF), and their combination, to induce neovascularization. Lack of endogenous FSAP in mice did not influence neovascularization. Thus, FSAP inhibited VEGF₁₆₅-mediated angiogenesis in the matrigel model in vivo, where VEGF’s interaction with the matrix and its diffusion are important. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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Review

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32 pages, 3133 KiB

Open AccessReview

Why Should Growth Hormone (GH) Be Considered a Promising Therapeutic Agent for Arteriogenesis? Insights from the GHAS Trial

by Diego Caicedo, Pablo Devesa, Clara V. Alvarez and Jesús Devesa

Cells 2020, 9(4), 807; https://doi.org/10.3390/cells9040807 - 27 Mar 2020

Cited by 11 | Viewed by 3608

Abstract

Despite the important role that the growth hormone (GH)/IGF-I axis plays in vascular homeostasis, these kind of growth factors barely appear in articles addressing the neovascularization process. Currently, the vascular endothelium is considered as an authentic gland of internal secretion due to the wide variety of released factors and functions with local effects, including the paracrine/autocrine production of GH or IGF-I, for which the endothelium has specific receptors. In this comprehensive review, the evidence involving these proangiogenic hormones in arteriogenesis dealing with the arterial occlusion and making of them a potential therapy is described. All the elements that trigger the local and systemic production of GH/IGF-I, as well as their possible roles both in physiological and pathological conditions are analyzed. All of the evidence is combined with important data from the GHAS trial, in which GH or a placebo were administrated to patients suffering from critical limb ischemia with no option for revascularization. We postulate that GH, alone or in combination, should be considered as a promising therapeutic agent for helping in the approach of ischemic disease. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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15 pages, 567 KiB

Open AccessReview

Arteriogenesis of the Spinal Cord—The Network Challenge

by Florian Simon, Markus Udo Wagenhäuser, Albert Busch, Hubert Schelzig and Alexander Gombert

Cells 2020, 9(2), 501; https://doi.org/10.3390/cells9020501 - 22 Feb 2020

Cited by 15 | Viewed by 6400

Abstract

Spinal cord ischemia (SCI) is a clinical complication following aortic repair that significantly impairs the quality and expectancy of life. Despite some strategies, like cerebrospinal fluid drainage, the occurrence of neurological symptoms, such as paraplegia and paraparesis, remains unpredictable. Beside the major blood supply through conduit arteries, a huge collateral network protects the central nervous system from ischemia—the paraspinous and the intraspinal compartment. The intraspinal arcades maintain perfusion pressure following a sudden inflow interruption, whereas the paraspinal system first needs to undergo arteriogenesis to ensure sufficient blood supply after an acute ischemic insult. The so-called steal phenomenon can even worsen the postoperative situation by causing the hypoperfusion of the spine when, shortly after thoracoabdominal aortic aneurysm (TAAA) surgery, muscles connected with the network divert blood and cause additional stress. Vessels are a conglomeration of different cell types involved in adapting to stress, like endothelial cells, smooth muscle cells, and pericytes. This adaption to stress is subdivided in three phases—initiation, growth, and the maturation phase. In fields of endovascular aortic aneurysm repair, pre-operative selective segmental artery occlusion may enable the development of a sufficient collateral network by stimulating collateral vessel growth, which, again, may prevent spinal cord ischemia. Among others, the major signaling pathways include the phosphoinositide 3 kinase (PI3K) pathway/the antiapoptotic kinase (AKT) pathway/the endothelial nitric oxide synthase (eNOS) pathway, the Erk1, the delta-like ligand (DII), the jagged (Jag)/NOTCH pathway, and the midkine regulatory cytokine signaling pathways. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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12 pages, 744 KiB

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Exercise-Induced Vascular Adaptations under Artificially Versus Pathologically Reduced Blood Flow: A Focus Review with Special Emphasis on Arteriogenesis

by Johanna Vogel, Daniel Niederer, Georg Jung and Kerstin Troidl

Cells 2020, 9(2), 333; https://doi.org/10.3390/cells9020333 - 31 Jan 2020

Cited by 8 | Viewed by 3498

Abstract

Background: The vascular effects of training under blood flow restriction (BFR) in healthy persons can serve as a model for the exercise mechanism in lower extremity arterial disease (LEAD) patients. Both mechanisms are, inter alia, characterized by lower blood flow in the lower limbs. We aimed to describe and compare the underlying mechanism of exercise-induced effects of disease- and external application-BFR methods. Methods: We completed a narrative focus review after systematic literature research. We included only studies on healthy participants or those with LEAD. Both male and female adults were considered eligible. The target intervention was exercise with a reduced blood flow due to disease or external application. Results: We identified 416 publications. After the application of inclusion and exclusion criteria, 39 manuscripts were included in the vascular adaption part. Major mechanisms involving exercise-mediated benefits in treating LEAD included: inflammatory processes suppression, proinflammatory immune cells, improvement of endothelial function, remodeling of skeletal muscle, and additional vascularization (arteriogenesis). Mechanisms resulting from external BFR application included: increased release of anabolic growth factors, stimulated muscle protein synthesis, higher concentrations of heat shock proteins and nitric oxide synthase, lower levels in myostatin, and stimulation of S6K1. Conclusions: A main difference between the two comparators is the venous blood return, which is restricted in BFR but not in LEAD. Major similarities include the overall ischemic situation, the changes in microRNA (miRNA) expression, and the increased production of NOS with their associated arteriogenesis after training with BFR. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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22 pages, 1257 KiB

Open AccessReview

An Emerging Role for isomiRs and the microRNA Epitranscriptome in Neovascularization

by Reginald V.C.T. van der Kwast, Paul H.A. Quax and A. Yaël Nossent

Cells 2020, 9(1), 61; https://doi.org/10.3390/cells9010061 - 25 Dec 2019

Cited by 27 | Viewed by 5035

Abstract

Therapeutic neovascularization can facilitate blood flow recovery in patients with ischemic cardiovascular disease, the leading cause of death worldwide. Neovascularization encompasses both angiogenesis, the sprouting of new capillaries from existing vessels, and arteriogenesis, the maturation of preexisting collateral arterioles into fully functional arteries. Both angiogenesis and arteriogenesis are highly multifactorial processes that require a multifactorial regulator to be stimulated simultaneously. MicroRNAs can regulate both angiogenesis and arteriogenesis due to their ability to modulate expression of many genes simultaneously. Recent studies have revealed that many microRNAs have variants with altered terminal sequences, known as isomiRs. Additionally, endogenous microRNAs have been identified that carry biochemically modified nucleotides, revealing a dynamic microRNA epitranscriptome. Both types of microRNA alterations were shown to be dynamically regulated in response to ischemia and are able to influence neovascularization by affecting the microRNA’s biogenesis, or even its silencing activity. Therefore, these novel regulatory layers influence microRNA functioning and could provide new opportunities to stimulate neovascularization. In this review we will highlight the formation and function of isomiRs and various forms of microRNA modifications, and discuss recent findings that demonstrate that both isomiRs and microRNA modifications directly affect neovascularization and vascular remodeling. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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13 pages, 683 KiB

Open AccessReview

Atherosclerosis and the Capillary Network; Pathophysiology and Potential Therapeutic Strategies

by Tilman Ziegler, Farah Abdel Rahman, Victoria Jurisch and Christian Kupatt

Cells 2020, 9(1), 50; https://doi.org/10.3390/cells9010050 - 24 Dec 2019

Cited by 46 | Viewed by 7925

Abstract

Atherosclerosis and associated ischemic organ dysfunction represent the number one cause of mortality worldwide. While the key drivers of atherosclerosis, arterial hypertension, hypercholesterolemia and diabetes mellitus, are well known disease entities and their contribution to the formation of atherosclerotic plaques are intensively studied and well understood, less effort is put on the effect of these disease states on microvascular structure an integrity. In this review we summarize the pathological changes occurring in the vascular system in response to prolonged exposure to these major risk factors, with a particular focus on the differences between these pathological alterations of the vessel wall in larger arteries as compared to the microcirculation. Furthermore, we intend to highlight potential therapeutic strategies to improve microvascular function during atherosclerotic vessel disease. Full article

(This article belongs to the Special Issue Arteriogenesis and Therapeutic Neovascularization)

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