Evidence map›Paper›PMID 40293549›Full record

ArticleJournal of molecular histology2025

STAT3/FoxO3a/Sirt1 pathway inhibition by ginsenoside Rc ameliorates cardiomyocyte damage in septic cardiomyopathy by altering macrophage polarization.

M S Jinzhong Wang, M S Jian Fu

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Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

2 authors.

M S Jinzhong Wang *Department of Critical Care Medicine, The Second Affiliated Hospital of Hainan Medical University, No. 48. Baishuitang Road, Haikou City, Hainan province, 570311, China. wjzh269@126.com.
M S Jian Fu *Department of Infectious Disease, Hainan General Hospital, Hainan Medical University, Haikou, Hainan, 570311, China.

Funding

Hainan Provincial Natural Science Foundation of China 820QN405
6 · The paper itself

Abstract

This study explored the role and mechanism of action of ginsenoside Rc in treating septic cardiomyopathy. Ginsenoside Rc mitigated LPS-induced oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction in cardiomyocytes and inhibited M1 polarization in macrophages. Ginsenoside Rc reduced the stimulating effect of M1-polarized macrophages on LPS-induced cardiomyocyte injury. Network pharmacological analysis suggested that ginsenoside Rc may play a role in septic cardiomyopathy through modulation of the STAT3/FoxO3a/Sirt1 pathway, which was validated in in vitro experiments. Ginsenoside Rc suppressed the expression of STAT3/FoxO3a pathway proteins and upregulated Sirt1. Moreover, influences of ginsenoside Rc on LPS-induced cardiomyocyte injury and macrophage polarization were abolished by ML115, a STAT3 agonist. In vivo, ginsenoside Rc notably improved myocardial injury and attenuated macrophage activation and inflammation in septic mice. Collectively, Ginsenoside Rc can ameliorate septic cardiomyopathy by modulating the STAT3/FoxO3a/Sirt1 pathway and altering macrophage polarization.

Indexed as

CardiomyopathiesForkhead Box Protein O3GinsenosidesMacrophagesMyocytes, CardiacSepsisSignal TransductionSirtuin 1STAT3 Transcription FactorAnimalsApoptosisLipopolysaccharidesMaleMiceMice, Inbred C57BLOxidative StressForkhead Box Protein O3FoxO3 protein, mouseGinsenosidesLipopolysaccharidesSirt1 protein, mouseSirtuin 1Stat3 protein, mouseSTAT3 Transcription FactorGinsenoside RcMacrophage polarizationMitochondrial dysfunctionSeptic cardiomyopathySTAT3

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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 OpenQuestion graph.