Animal and preliminary human studies of adult cell therapy following acute myocardial infarction have shown an overall improvement of cardiac function. Myocardial and vascular regeneration have been initially proposed as mechanisms of stem cell action. However, in many cases, the frequency of stem cell engraftment and the number of newly generated cardiomyocytes and vascular cells, either by transdifferentiation or cell fusion, appear too low to explain the significant cardiac improvement described. Accordingly, we and others have advanced an alternative hypothesis: the transplanted stem cells release soluble factors that, acting in a paracrine fashion, contribute to cardiac repair and regeneration. Indeed, cytokines and growth factors can induce cytoprotection and neovascularization. It has also been postulated that paracrine factors may mediate endogenous regeneration via activation of resident cardiac stem cells. Furthermore, cardiac remodeling, contractility, and metabolism may also be influenced in a paracrine fashion. This article reviews the potential paracrine mechanisms involved in adult stem cell signaling and therapy.

Paracrine Mechanisms in Adult Stem Cell Signaling and Therapy

Despite advances in clinical management, cardiovascular disease remains the leading cause of death in America. While cardiomyocytes retain limited plasticity following maturation, the heart is grossly unable to recover from structural damage. Mesenchymal stem cell (MSC) therapy, through its promise of repair and regeneration of cardiac tissue, represents an exciting avenue of treatment for a range of cardiovascular diseases. MSCs are relatively immunoprivileged, lacking both major histocompatibility II and T-cell co-stimulatory signal expression, and possess the unique ability to home into sites of myocardial damage when delivered systemically. Additionally, they have been shown to provide therapeutic benefit via several distinct mechanisms, the most important of which appears to be the abundant secretion of paracrine factors that promote local regeneration. In light of this, several groups have sought to precondition MSCs, using various molecular and genetic means, in order to enhance viability and growth factor secretion in the heart, following transplantation. Here, we analyze and integrate information from recent MSC studies, focusing on underlying mechanisms of MSC-associated repair in animal models of cardiac disease. Additionally, MSC pretreatment studies are organized here to examine their relative effectiveness and potential for clinical use. Data emerging from ongoing human clinical trials are also evaluated for consistency with animal studies and their therapeutic promise. Finally, we attempt to answer whether cumulative evidence from animal and human studies is suggestive of significant, clinically viable cardiac repair in acute and chronic conditions and explore ways in which future studies can enhance effectiveness of cell-based therapy.

Mesenchymal Stem Cell Therapy for Treatment of Cardiovascular Disease: Helping People Sooner or Later

Endothelial dysfunction is associated with major causes of morbidity and mortality, as well as numerous age-related conditions. The possibility of preserving or even rejuvenating endothelial function offers a potent means of preventing/treating some of the most fearful aspects of aging such as loss of mental, cardiovascular, and sexual function.

/pdf/circulating-endothelial-progenitor-cells-a-new-approach-to-21sakg10kq.pdf

Circulating endothelial progenitor cells: a new approach to anti-aging medicine?

Differential effect of myocardial matrix and integrins on cardiac differentiation of human mesenchymal stem cells

Regenerative medicine holds great promise as a way of addressing the limitations of current treatments of ischaemic disease In preclinical models, transplantation of different types of stem cells or progenitor cells results in improved recovery from ischaemia Furthermore, experimental studies indicate that cell therapy influences a spectrum of processes, including neovascularization and cardiomyogenesis as well as inflammation, apoptosis and interstitial fibrosis Thus, distinct strategies might be required for specific regenerative needs Nonetheless, clinical studies have so far investigated a relatively small number of options, focusing mainly on the use of bone marrow-derived cells Rapid clinical translation resulted in a number of small clinical trials that do not have sufficient power to address the therapeutic potential of the new approach Moreover, full exploitation has been hindered so far by the absence of a solid theoretical framework and inadequate development plans This article reviews the current knowledge on cell therapy and proposes a model theory for interpretation of experimental and clinical outcomes from a pharmacological perspective Eventually, with an increased association between cell therapy and traditional pharmacotherapy, we will soon need to adopt a unified theory for understanding how the two practices additively interact for a patient's benefit

LINKED ARTICLES
This article is part of a themed section on Regenerative Medicine and Pharmacology: A Look to the Future To view the other articles in this section visit http://dxdoiorg/101111/bph2013169issue-2

/pdf/stem-cell-therapy-for-cardiovascular-disease-the-demise-of-2qra45lk5i.pdf

Stem cell therapy for cardiovascular disease: the demise of alchemy and rise of pharmacology.

https://www.exphem.org/article/S0301-472X(06)00748-X/pdf

GFP-transduced CD34+ and Lin- CD34- hematopoietic stem cells did not adopt a cardiac phenotype in a nonhuman primate model of myocardial infarct.

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GFP-transduced CD34+ and Lin- CD34- hematopoietic stem cells did not adopt a cardiac phenotype in a nonhuman primate model of myocardial infarct.