Abstract
Oxidative stress and inflammation play major roles in the pathogenesis of coronary heart disease including myocardial infarction (MI). The pathological progression following MI is very complex and involves a number of cell populations including cells localized within the heart, as well as cells recruited from the circulation and other tissues that participate in inflammatory and reparative processes. These cells, with their secretory factors, have pleiotropic effects that depend on the stage of inflammation and regeneration. Excessive inflammation leads to enlargement of the infarction site, pathological remodeling and eventually, heart dysfunction. Stem cell therapy represents a unique and innovative approach to ameliorate oxidative stress and inflammation caused by ischemic heart disease. Consequently, it is crucial to understand the crosstalk between stem cells and other cells involved in post-MI cardiac tissue repair, especially immune cells, in order to harness the beneficial effects of the immune response following MI and further improve stem cell-mediated cardiac regeneration. This paper reviews the recent findings on the role of antioxidation and immunomodulation in postnatal multipotent stem cell-mediated cardiac repair following ischemic heart disease, particularly acute MI and focuses specifically on mesenchymal, muscle and blood-vessel-derived stem cells due to their antioxidant and immunomodulatory properties.
Highlights
Cardiovascular disease is the leading cause of mortality in the world with over 17 million deaths in 2008 alone [1], which is estimated to increase to over 23 million by 2030 and to remain the leading cause of deaths [2]
TNF-α stimulated PCs activated both neutrophils and monocytes to up-regulate mRNA expression of Toll-like receptor (TLR), matrix metalloproteases (MMP) and integrins as well as increased the surface expression of CD69 on monocytes, CD11b on neutrophils and extended neutrophil survival [123,124]. These experiments indicate that PCs express pattern recognition receptors to danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) and their activation causes the secretion of cytokines and chemokines, some of which are capable of activating neutrophils and monocytes, and influencing their migration which demonstrates the important role of PCs in innate immunity
The lack of oxygen and nutrients following myocardial infarction (MI) triggers a complex and dynamic process that involves the resident cells at the site of infarction, as well as the recruited cells from the circulation and other organs, generating inflammation and oxidative stress and further causing cardiac tissue damage, repair and heart remodeling
Summary
Cardiovascular disease is the leading cause of mortality in the world with over 17 million deaths in 2008 alone [1], which is estimated to increase to over 23 million by 2030 and to remain the leading cause of deaths [2]. Coronary heart disease causes the majority of deaths in cardiovascular disease with myocardial infarction (MI) often leading to the development of heart failure. MI is caused by occlusion of a coronary artery, which leads to a deficiency of oxygen and nutrients at the site of infarction and the subsequent death of cardiomyocytes. MI due to the ability of stem cells and/or their secretory factors to influence host cell migration, cellular functions, cardiomyocyte survival, tissue regeneration and healing [7,8,9]. The use of stem cells and/or their secretory factors may lead to effective therapeutic approaches for reducing the infarct size, generating more functional heart tissue, eliminating heart failure and improving the life of patients who have suffered from MI. The current review highlights the role of oxidative stress and the immune system in pathogenesis of acute MI and focuses on mesodermal stem cells, including mesenchymal, muscle and blood-vessel-derived stem cells, due to their antioxidant and immunomodulatory properties
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