Th17 response promotes angiotensin II-induced atherosclerosis

Med Hypotheses. 2011 Apr;76(4):593-5. doi: 10.1016/j.mehy.2011.01.008. Epub 2011 Feb 2.

Abstract

Vascular wall chronic inflammation plays a critical role in the development and progression of cardiovascular diseases such as atherosclerosis and hypertension. Circulating and tissue angiotensin II can induce potent inflammatory responses in vascular cells and promotes atherosclerosis, whereas the underlying mechanisms remain uncertain. Several data indicated that the upregulation of Th17 response has been found in the local atherosclerotic lesions and circulating lymphocytes in atherosclerosis prone models and the onset of acute coronary syndrome. Evidence from animal models shown that angiotensin II not only induced the Th1 response, but also amplified Th17 response. In addition, angiotensin II-induced hypertension and vascular dysfunction were abolished by blocking Th17/IL-17 effects. Therefore, we hypothesized that Th17 response may play an important role in angiotensin II-induced atherosclerosis.

MeSH terms

  • Angiotensin II / genetics
  • Angiotensin II / physiology*
  • Animals
  • Apolipoproteins E / genetics
  • Atherosclerosis / immunology*
  • Humans
  • Interleukin-18 / genetics
  • Mice
  • Mice, Mutant Strains
  • Th17 Cells / immunology*

Substances

  • Apolipoproteins E
  • Interleukin-18
  • Angiotensin II