Article citationsMore>>

N. Marx, T. Bourcier, G. K. Sukhova, et al., “PPARγ Activation in Human Endothelial Cells Increases Plasminogen Activator Inhibitor Type-1 Expression. PPARγ as a Potential Mediator in Vascular Disease,” Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 19, No. 3, 1999, pp. 546-551. doi:10.1161/01.ATV.19.3.546

has been cited by the following article:

• TITLE: PPAR and Local Renin-Angiotensin Systems in Cardiovascular and Metabolic Diseases Associated with Obesity: A Unifying Hypothesis

  AUTHORS: Gustavo Márquez-Salom, Javier Diez

  KEYWORDS: PPAR; Obesity; Diabetes; RAAS; Insulin

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.3 No.5A, August 15, 2013

  ABSTRACT: Recent research has revealed roles for the PPAR family of transcription factors in the modulation of the RAAS. In particular, PPARα and PPARγ have been shown to control the transcription of renin in several tissues and influence the activity of local renin-angiotensin-systems coupling vascular and metabolic functions and contributing to their modulation. In this conceptual framework, PPAR and local RAS participate in the pathophysiology of blood pressure elevation, as well as in organ and tissue damage, and disturbances of glucose and lipid metabolism associated with cardiovascular diseases and obesity. The understanding of these mechanisms here discussed and their adequate pharmacological manipulation enlarge the potential to intervene pathological processes that connect the obesity with associate diseases and could alert about the adverse effects of some PPAR agonists on involved organs.