Key result
Emodin improves LVEF and reduces cardiac injury markers in preclinical myocardial injury models.
Why the study?
Emodin has shown cardioprotective potential in animal models of myocardial injury, but the evidence is dispersed across small preclinical studies.
Does emodin reduce biochemical markers of myocardial injury and improve left ventricular systolic function compared with vehicle controls in preclinical animal models of myocardial injury?
Meta-Analysis (n=262)
Insufficiently described across included studies
Most included studies rated at low risk for sequence generation; allocation concealment insufficiently described
Does emodin reduce biochemical markers of myocardial injury and improve left ventricular systolic function compared with vehicle controls in preclinical animal models of myocardial injury?
In a meta-analysis of 16 preclinical animal studies, emodin significantly reduced myocardial injury biomarkers (CK, CK-MB, LDH) and improved cardiac systolic function (LVEF, LVSF), though high heterogeneity, risk of bias, and potential publication bias require resolution before clinical translation.
Answers are grounded in this paper and cite their sources.
Emodin may confer preclinical cardioprotection; hypothesis-generating for human translation and should not yet change practice.
Background Emodin, a plant-derived anthraquinone, has shown cardioprotective potential in animal models, but the evidence is dispersed across small preclinical studies. Methods PubMed, CNKI, Embase, and Web of Science were searched from inception to June 18, 2026, for controlled animal studies comparing emodin with vehicle controls in myocardial injury models. Continuous outcomes were pooled using random-effects models and expressed as standardized mean differences (SMDs) with 95% confidence intervals (CIs). Heterogeneity was assessed via I 2 . Leave-one-out analyses assessed robustness, and exploratory subgroup analyses examined heterogeneity. Egger's regression test assessed funnel plot asymmetry for outcomes with at least 10 studies. The protocol was registered with PROSPERO (CRD420261389730). Results Sixteen studies involving 262 animals were included. Emodin significantly reduced creatine kinase (CK, SMD = −11.83, 95% CI: −13.78 to −9.87, I 2 = 0%), creatine kinase-MB isoenzyme (CK-MB, SMD = −7.42, 95% CI: −10.05 to −4.78, I 2 = 83.0%), and lactate dehydrogenase (LDH, SMD = −10.03, 95% CI: −15.52 to −4.55, I 2 = 85.5%). Concomitantly, it improved left ventricular ejection fraction (LVEF, SMD = 5.35,95% CI: 2.76 to 7.94, I 2 = 81.0%) and left ventricular shortening fraction (LVSF, SMD = 3.59, 95% CI: 2.54 to 4.63, I 2 = 0%). Pooled effect directions remained unchanged in leave-one-out analyses. Sparse, correlated subgroups prevented reliable attribution of heterogeneity to individual study characteristics. The LVEF funnel plot was asymmetric. Trim-and-fill imputed two studies, after which the pooled LVEF effect was no longer statistically significant (SMD = 3.50, 95% CI: −0.28 to 7.28; P = 0.07). Conclusions This study suggests that emodin may reduce markers of myocardial injury and improve cardiac function. However, small sample sizes, risk of bias, and heterogeneity among the included studies limit confidence in these findings. Before clinical studies begin, pharmacokinetic research should clarify how exposure to emodin and its metabolites relates to pharmacodynamic effects. Systematic Review Registration : https://www.crd.york.ac.uk/PROSPERO/view/CRD420261389730 , identifier CRD420261389730.
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Chen et al. (2026) conducted a meta-analysis in Myocardial injury (preclinical animal models) (n=262). Emodin vs. Vehicle control (normal saline or unspecified control) was evaluated on Left ventricular ejection fraction (LVEF) (SMD 5.35, 95% CI 2.76 to 7.94). Emodin improved LVEF and reduced CK and CK-MB in preclinical myocardial injury models.
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