Abstract
Over the past several decades, stem cell therapy for heart disease has been translated from the bench to the bedside and in clinical trials improves cardiac structure and function in both ischemic and nonischemic cardiac disease. Although the regenerative effects of stem cells in cardiac disease are mediated by both paracrine and cell-to-cell contact mechanisms, many of the downstream signaling pathways remain to be fully elucidated. This review outlines what is currently known about the main signaling pathways involved in mesenchymal stem cell and cardiac stem cell survival, proliferation, and migration and mechanisms of action to repair the damaged heart.
Highlights
Ischemic heart disease remains the leading cause of death worldwide and has remained so for the past 15 years despite advances in medical therapy.[1]
Directions Stem cell therapy has evolved from in vitro studies to improvement in cardiac structure and function in both ischemic/nonischemic animal models and clinical trials
Regenerative effects are explained in large part by paracrine and cell-to-cell contact mechanisms
Summary
Ischemic heart disease remains the leading cause of death worldwide and has remained so for the past 15 years despite advances in medical therapy.[1]. Stromal-derived factor 1 treatment improved MSC migration and release of paracrine factors, both of which are vital to their therapeutic efficacy Inhibition of both the PI3K/ Akt and extracellular-regulated protein kinases 1/2 (ERK1/2) signaling pathways prevents the antiapoptotic effect of SDF-1 on MSCs under hypoxic conditions, indicating the importance of both of these pathways in SDF-1–mediated cell survival.[66]. Periostin is a cell adhesion protein that binds to integrins, is expressed by MSC and fibroblasts, and is upregulated in cardiac tissue undergoing remodeling in response to injury.[67] It has been shown to increase cardiomyocyte proliferation, migration, and adhesion via the PI3K pathway and recently has been implicated in improving MSC survival in an autocrine fashion. The mechanism remains to be elucidated, but it has been proposed that it is dependent on mitogen-activated protein kinase (MAPK) pathway.[83]
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