ReviewEXCLI journal2025
Prostaglandin E
Review in EXCLI journal, 2025. 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.
- Article
- Urine-Derived Stem Cells: Challenges in Isolation, Biological Identity, and Therapeutic Potential in CKD-Associated Fibrosis.International journal of molecular sciences · 2026Review
- Hormonal Dysregulation and Neuroinflammation in Endometriosis: Convergent Druggable Pathways.Current issues in molecular biology · 2026Review
- Distinct genetic architecture of gene and isoform level QTL in the Diversity Outbred (DO) mouse population.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostaglandin E₂ (PGE₂), which is traditionally recognized as a pro-inflammatory mediator target, is now recognized for its role in tissue regeneration. PGE₂ drives stem cell proliferation, M2 macrophage polarization, angiogenesis, and extracellular matrix (ECM) remodeling via E-type prostanoid (EP) receptor signaling, promoting repair in the skin, muscle, bone, heart, liver, kidney, and intestine. Despite these promising effects, the clinical translation of PGE₂ has been hindered by challenges such as a short half-life due to rapid degradation by 15-hydroxyprostaglandin dehydrogenase (15-PGDH), limited EP receptor subtype specificity, or oncogenic risks in certain contexts. This review explores the regenerative mechanisms of PGE₂, its tissue-specific roles, and innovative strategies to optimize therapeutic efficacy while minimizing adverse effects in regenerative medicine. See also the graphical abstract(Fig. 1).
Indexed as
Identifiers
What Socratic 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 Socratic graph.