Cellular and molecular mechanisms of inflammation-induced angiogenesis

IUBMB Life. 2015 Mar;67(3):145-59. doi: 10.1002/iub.1358. Epub 2015 Apr 21.

Abstract

Blood vessel formation is a fundamental process for the development of organism and tissue regeneration. Of importance, angiogenesis occurring during postnatal development is usually connected with inflammation. Here, we review how molecular and cellular mechanisms underlying inflammatory reactions regulate angiogenesis. Inflamed tissues are characterized by hypoxic conditions and immune cell infiltration. In this review, we describe an interplay of hypoxia-inducible factors (HIFs), HIF1 and HIF2, as well as NF-κB and nitric oxide in the regulation of angiogenesis. The mobilization of macrophages and the differential role of M1 and M2 macrophage subsets in angiogenesis are also discussed. Next, we present the current knowledge about microRNA regulation of inflammation in the context of new blood vessel formation. Finally, we describe how the mechanisms involved in inflammation influence tumor angiogenesis. We underlay and discuss the role of NF-E2-related factor 2/heme oxygenase-1 pathway as crucial in the regulation of inflammation-induced angiogenesis.

Keywords: HIF; NF-κB; Nrf2; heme oxygenase-1; hypoxia; microRNA; tumor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Hypoxia / physiology
  • Chemokine CCL2 / genetics
  • Chemokine CCL2 / metabolism
  • Gene Expression Regulation
  • Heme Oxygenase-1 / genetics
  • Heme Oxygenase-1 / metabolism
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Inflammation / genetics
  • Inflammation / physiopathology*
  • Ischemia / complications
  • Ischemia / physiopathology
  • Macrophages / metabolism
  • Macrophages / pathology
  • MicroRNAs
  • NF-E2-Related Factor 2 / genetics
  • NF-E2-Related Factor 2 / metabolism
  • NF-kappa B / metabolism
  • Neoplasms / blood supply
  • Neoplasms / physiopathology
  • Neovascularization, Pathologic / etiology*
  • Neovascularization, Pathologic / genetics
  • Neovascularization, Pathologic / metabolism
  • Signal Transduction

Substances

  • CCL2 protein, human
  • Chemokine CCL2
  • HIF1A protein, human
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • MicroRNAs
  • NF-E2-Related Factor 2
  • NF-kappa B
  • Heme Oxygenase-1