Human perivascular adipose tissue dysfunction as a cause of vascular disease: Focus on vascular tone and wall remodeling


Ozen G., Daci A., Norel X., Topal G.

EUROPEAN JOURNAL OF PHARMACOLOGY, cilt.766, ss.16-24, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Derleme
  • Cilt numarası: 766
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1016/j.ejphar.2015.09.012
  • Dergi Adı: EUROPEAN JOURNAL OF PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.16-24
  • Anahtar Kelimeler: Perivascular adipose tissue, Vascular tone, Vascular remodeling, Human, Obesity, Atherosclerosis, CORONARY-ARTERY-DISEASE, SAPHENOUS-VEIN GRAFT, INDUCED ENDOTHELIAL DYSFUNCTION, MUSCLE-CELL PROLIFERATION, RENIN-ANGIOTENSIN SYSTEM, NECROSIS-FACTOR-ALPHA, NITRIC-OXIDE, METABOLIC SYNDROME, INDUCED MIGRATION, OXIDATIVE STRESS
  • İstanbul Üniversitesi Adresli: Evet

Özet

Obesity is one of the major risk factors for the development of cardiovascular diseases. It is characterized by excessive or abnormal accumulation of adipose tissue, including depots which surround the blood vessels named perivascular adipose tissue (PVAT). PVAT plays endocrine and paracrine roles by producing large numbers of metabolically vasoactive adipokines. The present review outlines our current understanding of the beneficial roles of PVAT in vascular tone and remodeling in healthy subjects supported by clinical studies, highlighting different factors or mechanisms that could mediate protective effects of PVAT on vascular function. Most studies in humans show that adiponectin is the best candidate for the advantageous effect of PVAT. However, in pathological conditions especially obesity-related cardiovascular diseases, the beneficial effects of PVAT on vascular functions are impaired and transform into detrimental roles. This change is defined as PVAT dysfunction. In the current review, the contribution of PVAT dysfunction to obesity-related cardiovascular diseases has been discussed with a focus on possible mechanisms including an imbalance between beneficial and detrimental adipokines (commonly described as decreased levels of adiponectin and increased levels of leptin or tumor necrosis factor-alpha (TNR alpha)), increased quantity of adipose tissue, inflammation, cell proliferation and endothelial dysfunction. Finally, novel pharmacotherapeutic targets for the treatment of cardiovascular and metabolic disorders are addressed. (C) 2015 Elsevier B.V. All rights reserved.