Key result
Mesenchymal stem cell therapy shows safety and potential in reducing cardiac fibrosis and inflammation.
Why the study?
Many factors lead to cardiac fibrosis and failure, and an effective therapy is lacking to reverse or attenuate this condition.
Does mesenchymal stem cell therapy improve ventricular dysfunction and reduce cardiac fibrosis in ischemic and non-ischemic heart diseases?
Does mesenchymal stem cell therapy improve ventricular dysfunction and reduce cardiac fibrosis in ischemic and non-ischemic heart diseases?
This review highlights the immunomodulatory and anti-fibrotic mechanisms of mesenchymal stem cells, underscoring their therapeutic promise for treating heart failure while emphasizing the need for larger phase III trials.
Stem cell therapy is a promising alternative approach to heart diseases. The most prevalent source of multipotent stem cells, usually called somatic or adult stem cells (mesenchymal stromal/stem cells, MSCs) used in clinical trials is bone marrow (BM-MSCs), adipose tissue (AT-MSCs), umbilical cord (UC-MSCs) and placenta. Therapeutic use of MSCs in cardiovascular diseases is based on the benefits in reducing cardiac fibrosis and inflammation that compose the cardiac remodeling responsible for the maintenance of normal function, something which may end up causing progressive and irreversible dysfunction. Many factors lead to cardiac fibrosis and failure, and an effective therapy is lacking to reverse or attenuate this condition. Different approaches have been shown to be promising in surpassing the poor survival of transplanted cells in cardiac tissue to provide cardioprotection and prevent cardiac remodeling. This review includes the description of pre-clinical and clinical investigation of the therapeutic potential of MSCs in improving ventricular dysfunction consequent to diverse cardiac diseases.
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Gubert et al. (2021) conducted a review in Fibrotic Heart Diseases. Mesenchymal stem cells was evaluated. Mesenchymal stem cell therapy demonstrates safety and potential in reducing cardiac fibrosis and inflammation, improving ventricular dysfunction across pre-clinical models and early clinical trials.
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