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December 9, 2019Current Opinion in Nephrology & Hypertension

PPARγ is a gatekeeper for extracellular matrix and vascular cell homeostasis

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Why the study?

Activation of PPARγ improves mechanisms underlying pulmonary arterial hypertension, but reports on potential adverse effects of thiazolidinediones reduced clinical use over the past decade.

Do PPARγ agonists improve the pathobiological mechanisms of pulmonary arterial hypertension?

Design

Review

Authors

GKGábor KökényLCLaurent CalvierELEkaterina Legchenko

Discussion

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Overview

PPARγ activation may mitigate PAH mechanisms; leaves open clinical efficacy pending targeted trials.

Structured PICO

Do PPARγ agonists improve the pathobiological mechanisms of pulmonary arterial hypertension?

P
Population
Patients with pulmonary arterial hypertension (PAH) and preclinical models of vascular remodeling and tissue fibrosis
I
Intervention
PPARγ agonists (thiazolidinediones, specifically pioglitazone)
O
Outcome
Improvement in hallmarks of PAH (vascular remodeling, tissue fibrosis, BMPR2 dysfunction, inflammation)

Pharmacological activation of PPARγ with agents like pioglitazone improves multiple pathobiological mechanisms of PAH, suggesting a potential revival for their clinical use.

Cite This Study

Kökény et al. (2019) studied this question.

synapsesocial.com/papers/6a719ef56ceb2bbd16e0326dhttps://doi.org/10.1097/mnh.0000000000000580
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1KLF2-mediated disruption of PPAR-γ signaling in lymphatic endothelial cells exposed to chronically increased pulmonary lymph flow2018 · 18 citations
  2. 2Pulmonary Hypertension in Infants, Children, and Young Adults2017 · 179 citations
  3. 3Haemodynamic definitions and updated clinical classification of pulmonary hypertension2018 · 3,881 citations
  4. 4Reversing the curse on PPARγ2018 · 17 citations