Angiogenic cytokines in renovascular disease: do they have potential for therapeutic use?

J Am Soc Hypertens. 2013 Mar-Apr;7(2):180-90. doi: 10.1016/j.jash.2013.01.004. Epub 2013 Feb 19.

Abstract

Experimental and clinical studies suggest that the damage of the renal microvascular function and architecture may participate in the early steps of renal injury in chronic renal disease, irrespective of the cause. This supporting evidence has provided the impetus to targeting the renal microvasculature as an attempt to interfere with the progressive nature of the disease process. Chronic renovascular disease is often associated with renal microvascular dysfunction, damage, loss, and defective renal angiogenesis associated with progressive renal dysfunction and damage. It is possible that damage of the renal microvasculature in renovascular disease constitutes an initiating event for renal injury and contributes towards progressive and later on irreversible renal injury. Recent studies have suggested that protection of the renal microcirculation can slow or halt the progression of renal injury in this disease. This brief review will focus on the therapeutic potential and feasibility of using angiogenic cytokines to protect the kidney microvasculature in chronic renovascular disease. There is limited but provocative evidence showing that stimulation of vascular proliferation and repair using vascular endothelial growth factor or hepatocyte growth factor can slow the progression of renal damage, stabilize renal function, and protect the renal parenchyma. Such interventions may potentially constitute a sole strategy to preserve renal function and/or a co-adjuvant tool to improve the success of current therapeutic approaches in renovascular disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cytokines / pharmacology*
  • Disease Progression
  • Humans
  • Hypertension, Renovascular / drug therapy*
  • Hypertension, Renovascular / physiopathology
  • Microcirculation / drug effects*
  • Neovascularization, Physiologic / drug effects*

Substances

  • Cytokines