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Arteriogenesis, Angiogenesis and Vascular Remodeling, 2nd Edition

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Guest Editor
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
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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.

Blood flow restoration in arteries affected by atherosclerosis can also be achieved through balloon angioplasty, with or without stenting, or bypass surgery. Unfortunately, these interventions may also lead to the induction of vascular remodeling, leading to intimal hyperplasia and the re-occlusion of treated vessels. In these inflammatory-driven vascular remodeling processes, 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 vascular remodeling response in arteriogenesis and angiogenesis still need to be answered, and these answers will contribute to defining new therapeutic options.

Despite the substantial clinical potential of and many promising clinical trials on arteriogenesis and therapeutic angiogenesis, the exact molecular mechanisms involved in the multifactorial processes of vascular remodeling related to arteriogenesis and angiogenesis are still not completely understood.

This Special Issue of the International Journal of Molecular Sciences is devoted to all of the molecular aspects of arteriogenesis and collateral formation. It will contain articles that collectively provide balanced, state-of-the-art views on various aspects of arteriogenesis and the underlying regulation of vascular remodeling. We sincerely encourage you to read the papers published in Volume I (https://www.mdpi.com/journal/ijms/special_issues/Angiogenesis_Remodeling) and welcome your contributions to Volume II. 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, and therapeutic options. Potential topics include, but are not limited to, the following:

  • Genetic and environmental mechanisms controlling the formation and maintenance of native collateral circulation.
  • Mechanisms controlling pathophysiological formation and the maintenance of the angiogenic blood vessels.
  • Mechanisms controlling pathophysiological vascular remodeling.
  • Arteriogenesis, therapeutic angiogenesis, and peripheral arterial disease.
  • The formation of collateral arterial networks: insights from the developing embryo.
  • Multiple pathways converge in the development of collateral circulation.
  • Arteriogenesis and collateral formation.
  • Cell and gene therapy in peripheral arterial disease.
  • Epigenetic and epitranscriptomic mechanisms in arteriogenesis, angiogenesis, and vascular remodeling.
  • Non-coding RNA in vascular remodeling during arteriogenesis and angiogenesis.
  • Bone-marrow-derived cells in arteriogenesis and therapeutic angiogenesis.
  • Local and sustained drug delivery in arteriogenesis.
  • Mechanisms controlling arteriogenesis, angiogenesis, and vascular remodeling.

Prof. Dr. Paul Quax
Prof. Dr. Elisabeth Deindl
Guest Editors

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Keywords

  • arteriogenesis
  • angiogenesis
  • collateral formation
  • peripheral arterial disease
  • vascular remodeling
  • atherosclerosis
  • restenosis
  • intimal hyperplasia
  • vein grafting
  • cardiovascular diseases
  • cell and gene therapy
  • critical limb ischemia
  • therapeutic angiogenesis
  • collateral circulation
  • drug delivery

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Published Papers (1 paper)

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Research

9 pages, 2318 KiB  
Communication
Rag1 Deficiency Impairs Arteriogenesis in Mice
by Konda Kumaraswami, Christoph Arnholdt, Elisabeth Deindl and Manuel Lasch
Int. J. Mol. Sci. 2023, 24(16), 12839; https://doi.org/10.3390/ijms241612839 - 16 Aug 2023
Cited by 1 | Viewed by 1430
Abstract
Increasing evidence suggests that lymphocytes play distinct roles in inflammation-induced tissue remodeling and tissue damage. Arteriogenesis describes the growth of natural bypasses from pre-existing collateral arteries. This process compensates for the loss of artery function in occlusive arterial diseases. The role of innate [...] Read more.
Increasing evidence suggests that lymphocytes play distinct roles in inflammation-induced tissue remodeling and tissue damage. Arteriogenesis describes the growth of natural bypasses from pre-existing collateral arteries. This process compensates for the loss of artery function in occlusive arterial diseases. The role of innate immune cells is widely understood in the process of arteriogenesis, whereas the role of lymphocytes remains unclear and is the subject of the present study. To analyze the role of lymphocytes, we induced arteriogenesis in recombination activating gene-1 (Rag1) knockout (KO) mice by unilateral ligation of the femoral artery. The lack of functional lymphocytes in Rag1 KO mice resulted in reduced perfusion recovery as shown by laser Doppler imaging. Additionally, immunofluorescence staining revealed a reduced vascular cell proliferation along with a smaller inner luminal diameter in Rag1 KO mice. The perivascular macrophage polarization around the growing collateral arteries was shifted to more pro-inflammatory M1-like polarized macrophages. Together, these data suggest that lymphocytes are crucial for arteriogenesis by modulating perivascular macrophage polarization. Full article
(This article belongs to the Special Issue Arteriogenesis, Angiogenesis and Vascular Remodeling, 2nd Edition)
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