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

被引：75

作者：

la Sala, Andrea ^{[1
]}

Pontecorvo, Laura ^{[1
]}

Agresta, Alessia ^{[2
]}

Rosano, Giuseppe ^{[3
]}

Stabile, Eugenio ^{[2
]}

机构：

[1] IRCCS San Raffaele Pisana, Lab Mol & Cellular Immunol, I-00166 Rome, Italy

[2] Ctr Polidiagnost Stabile, I-84122 Salerno, Italy

[3] San Raffaele Sulmona, I-67039 Sulmona, Italy

来源：

TRENDS IN MOLECULAR MEDICINE | 2012年 / 18卷 / 08期

关键词：

arteriogenesis; T helper lymphocytes; regulatory T cells; macrophages; collateral vessel growth; ischemia; ENDOTHELIAL GROWTH-FACTOR; COLONY-STIMULATING FACTOR; ACUTE HINDLIMB ISCHEMIA; CD8(+) T-LYMPHOCYTES; ARTERY GROWTH; ARTERIOGENIC RESPONSE; FACTOR VEGF; MAST-CELLS; EXPRESSION; ANGIOGENESIS;

D O I：

10.1016/j.molmed.2012.06.007

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：494 / 501

页数：8

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