ArticleEuropean journal of histochemistry : EJH2025
Aloe-emodin ameliorates chronic kidney disease fibrosis by inhibiting PI3K-mediated signaling pathway.
Article in European journal of histochemistry : EJH, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Therapeutic effect of sustained release of aloe emodin via novel grafted polymer in electrospun nanofiber membranes on peritendinous adhesions.Frontiers in bioengineering and biotechnology · 2026Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) impacts a vast number of individuals worldwide, culminating in renal fibrosis. Renal fibrosis serves as the main reason for end-stage renal failure. However, the current targeted treatment methods for renal fibrosis remain scarce. Aloe-emodin (AE) is a naturally occurring compound discovered in rhubarb and aloe. In this research, we investigated the underlying mechanisms of AE in adenine-induced mouse renal fibrosis models and TGFβ-1 stimulated renal tubular epithelial cells (HK-2). It was discovered that AE not only decelerated the decline of renal function in adenine-treated mice but also suppressed the expression of Collagen I and Fibronectin. Furthermore, network pharmacology analysis suggested that AE's treatment of renal fibrosis might function via the PI3K/Akt/GSK3β signaling pathway. In vivo and in vitro Western blot and immunofluorescence findings demonstrate that AE significantly resists the advancement of renal fibrosis by inhibiting α-smooth muscle actin (α-SMA) and vimentin. Simultaneously, findings from 740Y-P (a PI3K agonist) and siRNA (PI3K) indicate that AE inhibits the expression of the PI3K/Akt/GSK3β cascade by lowering PI3K's phosphorylation level. From a mechanistic perspective, through molecular docking and plasmid transfection, the specific base sequence of PI3K in HK-2 cells was altered for experimental validation. The outcomes illustrate that AE can directly bind with PI3K, inhibiting its activation, impeding the PI3K/Akt/GSK3β signal transmission, thereby ultimately suppressing renal fibrosis progression. In conclusion, PI3K/Akt/GSK3β is a potential therapeutic target for CKD-related renal fibrosis, making AE a promising new treatment alternative for this condition.
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.