ArticleInternational journal of molecular sciences2026
Ellagic Acid Attenuates High-Fat, High-Sucrose Diet-Induced Cardiac Fibrosis by Suppressing AGE-RAGE Signaling, Oxidative Stress, and Inflammation.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
A high-fat, high-sucrose (HFHS) diet promotes insulin resistance and accelerates cardiac fibrosis (CF) through advanced glycation end products (AGEs), oxidative stress, and inflammation. Ellagic acid (EA) possesses antioxidant, anti-inflammatory, and anti-glycation properties; however, its protective effects against CF and underlying molecular mechanisms remain unclear. Therefore, we investigated EA's effects on HFHS-induced CF. Two-month-old male Wistar rats were randomly assigned to four groups (n = 6/group): control, control + 2% EA, HFHS, and HFHS + 2% EA, and maintained on respective diets for six months. Metabolic parameters, oxidative stress, AGE-related markers, histopathology, immunoblotting, and immunohistological analyses were performed. HFHS feeding induced metabolic dysfunction characterized by weight gain, increased fasting blood glucose levels, insulin resistance, dyslipidemia, myocardial disorganization, AGE accumulation, receptor for AGE (RAGE) activation, collagen deposition, and fibrotic marker expression- alpha smooth muscle actin (α-SMA). EA supplementation significantly improved metabolic abnormalities, reduced myocardial collagen fraction, AGE accumulation, RAGE activation, and α-SMA expression, thereby protecting against HFHS-induced CF.
Indexed as
Identifiers
What 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.