Evidence map›Paper›PMID 40313619›Full record

ArticleFrontiers in pharmacology2025

α-Mangostin prevents diabetic cardiomyopathy by inhibiting oxidative damage and lipotoxicity through the AKT-FOXO1-CD36 pathway.

Xue Bai, Ziqian Zhang, Miao Zhang, Jiaojiao Xu, Keting Dong, Qian Du, Lei Chen, Ping Ma, Jianhong Yang

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PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Xue BaiMedical School, University of Chinese Academy of Sciences, Beijing, China.
Ziqian ZhangMedical School, University of Chinese Academy of Sciences, Beijing, China.
Miao ZhangMedical School, University of Chinese Academy of Sciences, Beijing, China.
Jiaojiao XuMedical School, University of Chinese Academy of Sciences, Beijing, China.
Keting DongMedical School, University of Chinese Academy of Sciences, Beijing, China.
Qian DuMedical School, University of Chinese Academy of Sciences, Beijing, China.
Lei ChenMedical School, University of Chinese Academy of Sciences, Beijing, China.
Ping MaMedical School, University of Chinese Academy of Sciences, Beijing, China.
Jianhong YangMedical School, University of Chinese Academy of Sciences, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Diabetic cardiomyopathy (DCM), a cardiac complication of diabetes, is the main cause of the high prevalence of heart failure and associated mortality in diabetic patients. Oxidative stress and lipid metabolism disorder-induced myocardial cell damage are part of the pathogenesis of DCM. In this study, we investigated the effects of alpha-mangostin (A-MG), a natural antioxidant extracted from mangosteen peel, on Methods: H9C2 rat cardiomyocytes were treated with high glucose (HG) and palmitic acid (PA) for 24 h to establish an Results: In HG/F-induced H9C2 cells, A-MG (1 and 3 μM) significantly increased cell viability (p < 0.01) and reduced LDH release (p < 0.05). A-MG (3 μM) attenuated lipid accumulation (p < 0.05), normalized mitochondrial membrane potential (p < 0.01), and inhibited reactive oxygen species (ROS) generation (p < 0.05), malondialdehyde (MDA) production (p < 0.01), and apoptosis (p < 0.05). A-MG also inhibited the nuclear translocation of Forkhead box class O1 (FOXO1) (p < 0.05); reduced the expression of CD36 (p < 0.05), PPARα (p < 0.01), and CPT1β (p < 0.05) proteins; enhanced superoxide dismutase (SOD) activity (p < 0.05); and upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) (p < 0.01), HO-1 (p < 0.05), and SOD2 (p < 0.05) protein expression levels. Further investigation in HG/F-induced H9C2 cells indicated that A-MG inhibits the uptake of fatty acids (FAs) by regulating the AKT/FOXO1/CD36 signaling pathway, reduces excessive β-oxidation of FAs mediated by PPARα/CPT1β through the inhibition of FOXO1 nuclear translocation, and stimulates the AKT/Nrf2/HO-1 signaling pathway to increase the cellular antioxidant capacity. In diabetic mice, low-dose A-MG treatment increased anti-oxidative stress capacity, decreased myocardial lipid accumulation, reduced fibrosis and cardiomyocyte apoptosis, and improved left ventricular contractile function. Conclusion: Using both

Indexed as

alpha-mangostindiabetic cardiomyopathyforkhead box class O1lipotoxicityoxidative damage

Identifiers

PMID40313619
PMCPMC12043880

What Socratic holds

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Registered trials

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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.