Stem cell therapy following myocardial infarction generally demonstrates a decline in cardiac fibrosis, though the exact mechanisms remain unclear.
Does stem cell therapy reduce cardiac fibrosis and associated cardiac remodelling in experimental models of heart failure?
This review highlights that stem cell therapy reduces cardiac fibrosis in experimental models of myocardial infarction, though the exact mechanisms require further elucidation.
Cardiac fibrosis is a fundamental constituent of most cardiac pathologies and represents the upshot of nearly all types of cardiac injury. Generally, fibrosis is a scarring process, characterized by accumulation of fibroblasts and deposition of increasing amounts of extracellular matrix (ECM) proteins in the myocardium. Therapeutic approaches that control fibroblast activity and evade maladaptive processes could represent a potential strategy to attenuate progression towards heart failure. Currently, cell therapy is actively perceived as an alternative to traditional pharmacological management of myocardial infarction (MI). The majority of the studies applying stem cell therapy following MI have demonstrated a decline in fibrosis. However, it was not clearly recognized whether the decline in cardiac fibrosis was due to replacement of dead cardiomyocytes or because of the direct effects of paracrine factors released from the transplanted stem cells on the ECM. Therefore, the main focus of this review is to discuss the impact of different types of stem cells on cardiac fibrosis and associated cardiac remodelling in a variety of experimental models of heart failure, particularly MI.
Elnakish et al. (2012) conducted a review in Cardiac fibrosis and heart failure, particularly myocardial infarction. Stem cell transplantation was evaluated on Cardiac fibrosis and associated cardiac remodelling. Stem cell therapy following myocardial infarction generally demonstrates a decline in cardiac fibrosis, though the exact mechanisms remain unclear.