Heart regeneration, stem cells, and cytokines

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Abstract

The human heart has limited regenerative capacity, which makes the reparative response after the cardiac infarction quite challenging. During the last decade, stem cells have become promising candidates for heart repair, owing to their potent differentiation capacity and paracrine cytokine secretion. Among the different types of stem cells, mesenchymal stem cells have high proliferative potential and secrete numerous cytokines, growth factors, and microRNAs. The paracrine cytokines play important roles in cardiac regeneration, neovascularization, anti-apoptosis, and anti-remodeling mechanisms, among others. This review summarizes the cytokines secreted by stem cells and their relative signaling pathways, which represent key mechanisms for heart regeneration and may serve as a promising future therapeutic strategy for myocardial infarction patients.

Most cited references 53

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Adult cardiac stem cells are multipotent and support myocardial regeneration.

Antonio P Beltrami, Laura Barlucchi, Daniele Torella … (2003)

The notion of the adult heart as terminally differentiated organ without self-renewal potential has been undermined by the existence of a subpopulation of replicating myocytes in normal and pathological states. The origin and significance of these cells has remained obscure for lack of a proper biological context. We report the existence of Lin(-) c-kit(POS) cells with the properties of cardiac stem cells. They are self-renewing, clonogenic, and multipotent, giving rise to myocytes, smooth muscle, and endothelial cells. When injected into an ischemic heart, these cells or their clonal progeny reconstitute well-differentiated myocardium, formed by blood-carrying new vessels and myocytes with the characteristics of young cells, encompassing approximately 70% of the ventricle. Thus, the adult heart, like the brain, is mainly composed of terminally differentiated cells, but is not a terminally differentiated organ because it contains stem cells supporting its regeneration. The existence of these cells opens new opportunities for myocardial repair.

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Cell therapy for heart failure: a comprehensive overview of experimental and clinical studies, current challenges, and future directions.

Santosh K Sanganalmath, Roberto Bolli (2013)

Despite significant therapeutic advances, the prognosis of patients with heart failure (HF) remains poor, and current therapeutic approaches are palliative in the sense that they do not address the underlying problem of the loss of cardiac tissue. Stem cell-based therapies have the potential to fundamentally transform the treatment of HF by achieving what would have been unthinkable only a few years ago-myocardial regeneration. For the first time since cardiac transplantation, a therapy is being developed to eliminate the underlying cause of HF, not just to achieve damage control. Since the initial report of cell therapy (skeletal myoblasts) in HF in 1998, research has proceeded at lightning speed, and numerous preclinical and clinical studies have been performed that support the ability of various stem cell populations to improve cardiac function and reduce infarct size in both ischemic and nonischemic cardiomyopathy. Nevertheless, we are still at the dawn of this therapeutic revolution. Many important issues (eg, mechanism(s) of action of stem cells, long-term engraftment, optimal cell type(s), and dose, route, and frequency of cell administration) remain to be resolved, and no cell therapy has been conclusively shown to be effective. The purpose of this article is to critically review the large body of work performed with respect to the use of stem/progenitor cells in HF, both at the experimental and clinical levels, and to discuss current controversies, unresolved issues, challenges, and future directions. The review focuses specifically on chronic HF; other settings (eg, acute myocardial infarction, refractory angina) are not discussed.

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Bone marrow mesenchymal stem cells stimulate cardiac stem cell proliferation and differentiation.

Konstantinos E Hatzistergos, Henry Quevedo, Behzad Oskouei … (2010)

The regenerative potential of the heart is insufficient to fully restore functioning myocardium after injury, motivating the quest for a cell-based replacement strategy. Bone marrow-derived mesenchymal stem cells (MSCs) have the capacity for cardiac repair that appears to exceed their capacity for differentiation into cardiac myocytes. Here, we test the hypothesis that bone marrow derived MSCs stimulate the proliferation and differentiation of endogenous cardiac stem cells (CSCs) as part of their regenerative repertoire. Female Yorkshire pigs (n=31) underwent experimental myocardial infarction (MI), and 3 days later, received transendocardial injections of allogeneic male bone marrow-derived MSCs, MSC concentrated conditioned medium (CCM), or placebo (Plasmalyte). A no-injection control group was also studied. MSCs engrafted and differentiated into cardiomyocytes and vascular structures. In addition, endogenous c-kit(+) CSCs increased 20-fold in MSC-treated animals versus controls (P<0.001), there was a 6-fold increase in GATA-4(+) CSCs in MSC versus control (P<0.001), and mitotic myocytes increased 4-fold (P=0.005). Porcine endomyocardial biopsies were harvested and plated as organotypic cultures in the presence or absence of MSC feeder layers. In vitro, MSCs stimulated c-kit(+) CSCs proliferation into enriched populations of adult cardioblasts that expressed Nkx2-5 and troponin I. MSCs stimulate host CSCs, a new mechanism of action underlying successful cell-based therapeutics.

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Author and article information

Contributors

Na Li: lina82002@126.com

Chuan Wang: ts_kevin@hotmail.com

LiXin Jia: lixinjia1985@126.com

Jie Du: jiedubj@126.com

Journal

Journal ID (nlm-ta): Regen Med Res

Journal ID (iso-abbrev): Regen Med Res

Title: Regenerative Medicine Research

Publisher: BioMed Central (London )

ISSN (Electronic): 2050-490X

Publication date (Electronic): 2 April 2014

Publication date PMC-release: 2 April 2014

Publication date Collection: December 2014

Volume: 2

Issue: 1

Electronic Location Identifier: 6

Affiliations

[ ]Capital Medical University Affiliated Beijing Anzhen Hospital, Anzhenli, Chaoyang District, Beijing, 100029 China

[ ]Lung and Vessel Diseases, Beijing Research Institute of Heart, Beijing, 100029 China

[ ]The Key Laboratory of Remodeling-related Cardiovascular Diseases, Capital Medical University, Ministry of Education, Beijing, China

Article

Publisher ID: 10

DOI: 10.1186/2050-490X-2-6

PMC ID: 4390097

PubMed ID: 25984334

SO-VID: 861e962b-4905-4b62-8e2b-99a71b219b52

License:

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited.