Regulation of collateral blood vessel development by the innate and adaptive immune system

The development of collateral circulation is an inherent compensatory mechanism to restore impaired blood perfusion following artery stenosis and/or occlusion. This process, termed arteriogenesis, is driven by inflammation and involves a complex remodeling of pre-existing conduit vessels running in...

Full description

Saved in:
Bibliographic Details
Published in:Trends in molecular medicine 2012-08, Vol.18 (8), p.494-501
Main Authors: la Sala, Andrea, Pontecorvo, Laura, Agresta, Alessia, Rosano, Giuseppe, Stabile, Eugenio
Format: Article
Language:English
Subjects:
Adaptive Immunity
Animals
Arteries
arteriogenesis
Blood vessels
Blood Vessels - growth & development
Blood Vessels - immunology
Collateral Circulation
collateral vessel growth
Helper cells
Humans
Immune system
Immunity, Innate
Inflammation
ischemia
Lymphocytes - immunology
Lymphocytes T
Macrophages
Natural killer cells
Neovascularization, Pathologic - immunology
Neovascularization, Pathologic - physiopathology
Occlusion
Pathology
Perfusion
regulatory T cells
Reviews
Running
Stenosis
T helper lymphocytes
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The development of collateral circulation is an inherent compensatory mechanism to restore impaired blood perfusion following artery stenosis and/or occlusion. This process, termed arteriogenesis, is driven by inflammation and involves a complex remodeling of pre-existing conduit vessels running in parallel to the occluded artery. Recent studies have unveiled roles for different immune cell subsets as regulators of arteriogenesis, including natural killer (NK) cells, T helper 17 (Th17) cells, regulatory T lymphocytes (Tregs), and functional subsets of macrophages (e.g., M2 macrophages). This review summarizes recent findings and discusses future research needed to better define the time during which each cellular subset is active and reveal further critical regulatory switches.
ISSN:1471-4914
1471-499X
DOI:10.1016/j.molmed.2012.06.007