• Open Access

Repair mechanisms of bone marrow mesenchymal stem cells in myocardial infarction


Correspondence to: Jingfeng WANG, M.D. and Tong WANG, M.D.,Cardiovascular Medicine, The Sun Yat-sen Memorial Hospital of Sun Yat-sen University, 107 Yanjiang Xi Road, Guangzhou 510120, China.
Tel.: (8620)8133–2430
Fax: (8620)8133–2430
E-mail: Dr.wangjf@hotmail.com; tongwang163@yahoo.com.cn


  • • Introduction
  • • Transdifferentiation
    • - MSCs differentiate into cardiomyocytes
    • - MSCs differentiate into vascular cells
  • • Paracrine effects
    • - Endogenous cardiac regeneration induced by paracrine effects
    • - Neovascularization induced by paracrine effects
    • - Anti-inflammatory effect of MSCs
    • - Anti-apoptotic effects by MSCs
    • - Cardiac remodelling induced by paracrine effects
    • - Paracrine-mediated cardiac contractility
    • - Cardiac metabolic modulation by MSCs
  • • Other potential effects
    • - Cardiac nerve sprouting
    • - Anti-arrhythmic potential
  • • Conclusion

The prognosis of patients with myocardial infarction (MI) and resultant chronic heart failure remains extremely poor despite advances in optimal medical therapy and interventional procedures. Animal experiments and clinical trials using adult stem cell therapy following MI have shown a global improvement of myocardial function. Bone marrow-derived mesenchymal stem cells (MSCs) hold promise for cardiac repair following MI, due to their multilineage, self-renewal and proliferation potential. In addition, MSCs can be easily isolated, expanded in culture, and have immunoprivileged properties to the host tissue. Experimental studies and clinical trials have revealed that MSCs not only differentiate into cardiomyocytes and vascular cells, but also secrete amounts of growth factors and cytokines which may mediate endogenous regeneration via activation of resident cardiac stem cells and other stem cells, as well as induce neovascularization, anti-inflammation, anti-apoptosis, anti-remodelling and cardiac contractility in a paracrine manner. It has also been postulated that the anti-arrhythmic and cardiac nerve sprouting potential of MSCs may contribute to their beneficial effects in cardiac repair. Most molecular and cellular mechanisms involved in the MSC-based therapy after MI are still unclear at present. This article reviews the potential repair mechanisms of MSCs in the setting of MI.