ArticleExperimental and clinical cardiology2004
The possible role of peroxisome proliferator-activated receptor gamma in heart failure.
Article in Experimental and clinical cardiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Transcriptional regulatory network analysis uncovers modular gene control and potential key regulators in diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2026Article
- Role of PPAR-related genes in chronic heart failure: evidence from large populations.BMC cardiovascular disorders · 2023Article
- Review
- Rational screening of peroxisome proliferator-activated receptor-γ agonists from natural products: potential therapeutics for heart failure.Pharmaceutical biology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peroxisome proliferator-activated receptors (PPARs) are transcription factors belonging to the nuclear receptor superfamily that heterodimerize with the retinoid X receptor and bind to specific response elements in target gene promoters. PPARs have three isoforms: alpha, beta (or delta) and gamma. The prostaglandin D(2) metabolite, 15-deoxy-12,14-prostaglandin J(2), is an endogenous ligand for PPARgamma. The antidiabetic thiazolidinediones are synthetic ligands for PPARgamma. PPARgamma is expressed predominantly in adipose tissue and promotes adipocyte differentiation and glucose homeostasis. PPARgamma is also present in various cell types including cardiac myocytes. PPARgamma regulates various neurohumoral factors involved in the progression of heart failure; its ligands inhibit cardiac hypertrophy and ischemia-reperfusion injury via, in part, a PPAR-independent pathway. Although experimental studies suggest that PPARgamma ligands might have a favourable influence on heart failure, their use in patients with heart failure is limited because of an increase in plasma volume. Further studies are needed to determine whether PPARgamma ligands prevent the development of heart disease in clinical settings.
Indexed as
Identifiers
19641720PMC2716741W292478153What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.