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This anticontractile effect of PVAT is lost under conditions of obesity. The central mechanism underlying this PVAT dysfunction in obesity is likely to be an \u2018obesity triad\u2019 (consisting of PVAT hypoxia, inflammation and oxidative stress) that leads to the impairment of PVAT\u2010derived vasoregulators. The production of hydrogen sulfide, NO and adiponectin by PVAT is reduced in obesity, whereas the vasodilator response to leptin is impaired (vascular leptin resistance). Strikingly, the vasodilator response to acetylcholine is reduced only in PVAT\u2010containing, but not in PVAT\u2010free thoracic aorta isolated from diet\u2010induced obese mice, indicating a unique role for PVAT in obesity\u2010induced vascular dysfunction. Furthermore, PVAT dysfunction has also been observed in small arteries isolated from the gluteal\/visceral fat biopsy samples of obese individuals. Therefore, PVAT may represent a new therapeutic target for vascular complications in obesity. A number of approaches are currently being tested under experimental conditions. Potential therapeutic strategies improving PVAT function include body weight reduction, enhancing PVAT hydrogen sulfide release (e.g. rosiglitazone, atorvastatin and cannabinoid CB\n                      <jats:sub>1<\/jats:sub>\n                      receptor agonists) and NO production (e.g. arginase inhibitors), inhibition of the renin\u2013angiotensin\u2013aldosterone system, inhibition of inflammation with melatonin or cytokine antagonists, activators of AMP\u2010activated kinase (e.g. metformin, resveratrol and diosgenin) and adiponectin releasers or expression enhancers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Linked Articles<\/jats:title>\n                    <jats:p>\n                      This article is part of a themed section on Molecular Mechanisms Regulating Perivascular Adipose Tissue \u2013 Potential Pharmacological Targets? To view the other articles in this section visit\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v174.20\/issuetoc\">http:\/\/onlinelibrary.wiley.com\/doi\/10.1111\/bph.v174.20\/issuetoc<\/jats:ext-link>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/bph.13650","type":"journal-article","created":{"date-parts":[[2016,10,20]],"date-time":"2016-10-20T03:56:38Z","timestamp":1476935798000},"page":"3425-3442","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":187,"title":["The role of perivascular adipose tissue in obesity\u2010induced vascular dysfunction"],"prefix":"10.1111","volume":"174","author":[{"given":"Ning","family":"Xia","sequence":"first","affiliation":[{"name":"Department of Pharmacology Johannes Gutenberg University Medical Center  Mainz 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