RT Journal Article
T1 Antihypertensive effects of peroxisome proliferator-activated receptor-β/δ activation.
A1 Toral, Marta
A1 Romero, Miguel
A1 Perez-Vizcaino, Francisco
A1 Duarte, Juan
A1 Jimenez, Rosario
K1 PPARβ/δ
K1 endothelial dysfunction
K1 hypertension
K1 oxidative stress
K1 vascular remodeling
AB Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily of ligand-activated transcription factors, which is composed of three members encoded by distinct genes: PPARα, PPARβ/δ, and PPARγ. The biological actions of PPARα and PPARγ and their potential as a cardiovascular therapeutic target have been extensively reviewed, whereas the biological actions of PPARβ/δ and its effectiveness as a therapeutic target in the treatment of hypertension remain less investigated. Preclinical studies suggest that pharmacological PPARβ/δ activation induces antihypertensive effects in direct [spontaneously hypertensive rat (SHR), ANG II, and DOCA-salt] and indirect (dyslipemic and gestational) models of hypertension, associated with end-organ damage protection. This review summarizes mechanistic insights into the antihypertensive effects of PPARβ/δ activators, including molecular and functional mechanisms. Pharmacological PPARβ/δ activation induces genomic actions including the increase of regulators of G protein-coupled signaling (RGS), acute nongenomic vasodilator effects, as well as the ability to improve the endothelial dysfunction, reduce vascular inflammation, vasoconstrictor responses, and sympathetic outflow from central nervous system. Evidence from clinical trials is also examined. These preclinical and clinical outcomes of PPARβ/δ ligands may provide a basis for the development of therapies in combating hypertension.
PB American Physiological Society
YR 2016
FD 2016-11-21
LK http://hdl.handle.net/10668/10630
UL http://hdl.handle.net/10668/10630
LA en
NO Toral M, Romero M, Pérez-Vizcaíno F, Duarte J, Jiménez R. Antihypertensive effects of peroxisome proliferator-activated receptor-β/δ activation. Am J Physiol Heart Circ Physiol. 2017 Feb 1;312(2):H189-H200.
NO This work was supported by grants from Comisión Interministerial deCiencia y Tecnología (SAF2014 –55523-R, SAF2014 –55399R), Junta de An-dalucía (Proyecto de excelencia, P12-CTS-2722) with funds from the Euro-pean Union, Ministerio de Ciencia e Innovación Campus de ExcelenciaInternacional (Programa GREIB), Ministerio de Economía y Competitividad,and Instituto de Salud Carlos III (RIC RD12/0042/0011), Spain.
DS RISalud
RD Apr 19, 2025