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Updated: Jun 25, 2026

A Hydrogel Construct and Fibrin-based Glue Approach to Deliver Therapeutics in a Murine Myocardial Infarction Model.
Published on: June 14, 2015
A plant-derived remedy for repair of infarcted heart
Lei Cheng1, Hao Chen, Xinsheng Yao
1Key Laboratory for Regenerative Medicine of Ministry of Education of China, The Chinese University of Hong Kong, Hong Kong SAR, China.
Insights
A novel compound, cardiogenin, isolated from Geum japonicum extract, effectively regenerates heart tissue after myocardial infarction (MI). This discovery offers a promising new strategy for treating heart damage by activating mesenchymal stem cells (MSCs) for cardiogenic differentiation.
Area of Science:
- Cardiovascular Research
- Stem Cell Biology
- Pharmacology
Background:
- Myocardial infarction (MI) is a leading cause of death, with limited therapeutic options for regenerating damaged heart tissue.
- Current strategies using stem cells for myocardial regeneration face challenges due to low cardiogenic differentiation (CD) efficiency.
- Previous studies showed therapeutic effects of Geum japonicum (EGJ) extract in an acute MI model.
Purpose of the Study:
- To isolate the active component from EGJ responsible for myocardial regeneration.
- To investigate the efficacy of the isolated compound, cardiogenin, in treating MI.
- To elucidate the mechanisms underlying cardiogenin-induced myocardial repair and stem cell activation.
Main Methods:
- Bioassay-guided isolation of active compounds from EGJ extract.
- Administration of EGJ and isolated cardiogenin in animal MI models.
- Assessment of myocardial regeneration, stem cell differentiation, and cardiac function.
- Analysis of signaling pathways involved in cell survival, CD, and angiogenesis.
Main Results:
- Cardiogenin significantly repaired infarcted heart tissue in MI models, mimicking EGJ extract's effects.
- Newly regenerated cardiomyocytes derived from endogenous mesenchymal stem cells (MSCs) were observed in the infarct zone, improving heart function.
- Transplantation of EGJ or cardiogenin-pretreated MSCs led to substantial functional myocardium regeneration.
- Signaling pathways crucial for cell survival, CD, and angiogenesis were activated by cardiogenin.
Conclusions:
- Cardiogenin demonstrates significant therapeutic potential for infarcted heart repair.
- The study identified key signaling pathways enabling cardiogenic differentiation of MSCs, cell survival, and angiogenesis.
- These findings pave the way for developing novel treatment strategies for myocardial infarction.
Background:
Myocardial infarction (MI) due to coronary artery disease remains one of the leading causes of premature death. Replacement of infarcted heart tissue with regenerating myocardium from endogenous progenitor pools or exogenously introduced stem cells remains a therapeutic ideal. Their impracticality mainly lies in their low efficiency in cardiogenic differentiation (CD). Our recent studies with an acute MI animal model have already demonstrated the therapeutic effect of the MeOH extract of Geum japonicum (EGJ), providing clear evidence of myocardial regeneration.
Methods And Findings:
The present study further isolated the active component contained in EGJ using bioassay-guided isolation and investigated its efficacy in the treatment of infarcted heart in animal MI models. We demonstrated that substantial repair of infarcted heart in animal MI models by EGJ can be mimicked by the isolated candidate compound (cardiogenin) in MI animal models. Clear evidence of newly regenerated endogenous mesenchymal stem cells (MSCs) derived cardiomyocytes was observed throughout the infarct zone, accompanied by significantly improved functional performance of the heart. Transplantation of MSCs pretreated with EGJ or cardiogenin into a MI animal model also resulted in substantial regeneration of functional myocardium, implying that the activated MSCs carry all the necessary blueprints for myocardial regeneration. Signaling pathways specific to cell survival, CD identified in embryonic heart induction and angiogenesis were activated in both cardiogenin-treated MSCs and cardiogenin-induced regenerating myocardium.
Conclusions:
This study has demonstrated the therapeutic effects of cardiogenin in infarcted heart repair, and identified the associated signalling pathways for effective cardiogenic differentiation of MSCs, cell survival and angiogenesis. These findings should enable new treatment strategies for MI to be developed immediately.
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