ReviewCurrent medical science2026
Emodin: A Promising Natural Compound for Combating Fibrotic Diseases.
Review in Current medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
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.
Funding
Abstract
Fibrotic diseases place a substantial burden on health and the economy, with limited treatment options. Therefore, effective therapeutic strategies are urgently needed. Emodin, a natural compound with diverse biological activities, has been demonstrated in multiple studies over recent years to have potential therapeutic effects on fibrotic diseases. This review aims to provide a comprehensive overview of the existing research on emodin's pharmacological effects and mechanisms in inhibiting fibrotic disease, with a focus on its therapeutic advantages and systemic mechanisms. Recent studies have shown that emodin plays a role in combating fibrotic diseases by suppressing the production of inflammatory cytokines, such as IL-1β, IL-6, and TNF-α; it alleviates inflammation by inhibiting the NF-κB signaling pathway and preventing the degradation of IκB. Emodin also suppresses the activation of the MAPK pathway, enhances the expression of antioxidant enzymes, and influences the metabolism of the extracellular matrix (ECM). Thus, emodin is highlighted for its potential as an antifibrotic agent, and future research directions are proposed to deepen our understanding and develop novel treatment strategies for fibrotic diseases.
Indexed as
Identifiers
41505073What 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.