Combined Transplantation of Human MSCs and ECFCs Improves Cardiac Function and Decrease Cardiomyocyte Apoptosis After Acute Myocardial Infarction

Tripathi, Himi; Domingues, Alison; Donahue, Renée R.; Cras, Audrey; Guérin, Coralie L.; Gao, Erhe; Levitan, Bryana M.; Ratajczak, Mariusz Z.; Smadja, David; Abdel‐Latif, Ahmed; Tarhuni, Wadea

doi:10.1007/s12015-022-10468-z

Cited by 9 publications

(6 citation statements)

References 17 publications

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“…DREAM-HF, a phase III clinical trial, recruited 565 patients and upon completion will provide evidence in analyzing the efficiency of MSC injection as a heart failure treatment [ 14 , 134 , 135 ]. Recent studies show that human mesenchymal stromal cells and endothelial colony-forming cells reduce cardiomyocyte apoptosis, scar size, and adverse cardiac remodeling, compared to vehicle, in a pre-clinical model of acute myocardial infarction [ 136 ]. Human ESC-derived endothelial cells also attenuate cardiac remodeling in a mouse myocardial infarction model [ 137 ].…”

Section: Approaches and Challenges For Heart Regenerationmentioning

confidence: 99%

Regeneration of the heart: from molecular mechanisms to clinical therapeutics

et al. 2023

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Heart injury such as myocardial infarction leads to cardiomyocyte loss, fibrotic tissue deposition, and scar formation. These changes reduce cardiac contractility, resulting in heart failure, which causes a huge public health burden. Military personnel, compared with civilians, is exposed to more stress, a risk factor for heart diseases, making cardiovascular health management and treatment innovation an important topic for military medicine. So far, medical intervention can slow down cardiovascular disease progression, but not yet induce heart regeneration. In the past decades, studies have focused on mechanisms underlying the regenerative capability of the heart and applicable approaches to reverse heart injury. Insights have emerged from studies in animal models and early clinical trials. Clinical interventions show the potential to reduce scar formation and enhance cardiomyocyte proliferation that counteracts the pathogenesis of heart disease. In this review, we discuss the signaling events controlling the regeneration of heart tissue and summarize current therapeutic approaches to promote heart regeneration after injury.

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Section: Approaches and Challenges For Heart Regenerationmentioning

confidence: 99%

Regeneration of the heart: from molecular mechanisms to clinical therapeutics

et al. 2023

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“…An early study showed that the administration of ECFCs in a porcine model of AMI decreased the infarct size and increased microvessel density, which attenuated the adverse myocardial remodeling [38]. Another recent study demonstrated that the transplantation of ECFCs combined with mesenchymal stem cells (MSCs) into MI mice with permanent ligation of the left descendent coronary artery significantly improved cardiac function and alleviated the ischemic cardiac damage by increasing capillary density 30 days after AMI, although the underlying signaling pathways of this combined cell-therapy has not been addressed [39]. Likewise, a previous report indicated that the injection of ECFCs and MSCs into the infarcted heart of MI mice promoted a regenerative effect seemingly mediated by the upregulation of multiple paracrine factors associated with angiogenesis such as Ang-2, FGF-2, IGF-1, and SDF-1α [40].…”

Section: Reparative Role Of Mature and Endothelial Progenitor Cells I...mentioning

confidence: 99%

“…significantly improved cardiac function and alleviated the ischemic cardiac damage by increasing capillary density 30 days after AMI, although the underlying signaling pathways of this combined cell-therapy has not been addressed [39]. Likewise, a previous report indicated that the injection of ECFCs and MSCs into the infarcted heart of MI mice promoted a regenerative effect seemingly mediated by the upregulation of multiple paracrine factors associated with angiogenesis such as Ang-2, FGF-2, IGF-1, and SDF-1α [40].…”

Section: Reparative Role Of Mature and Endothelial Progenitor Cells I...mentioning

confidence: 99%

New Insights into the Reparative Angiogenesis after Myocardial Infarction

Martín-Bórnez,

Falcón,

Morrugares

et al. 2023

IJMS

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Myocardial infarction (MI) causes massive loss of cardiac myocytes and injury to the coronary microcirculation, overwhelming the limited capacity of cardiac regeneration. Cardiac repair after MI is finely organized by complex series of procedures involving a robust angiogenic response that begins in the peri-infarcted border area of the infarcted heart, concluding with fibroblast proliferation and scar formation. Efficient neovascularization after MI limits hypertrophied myocytes and scar extent by the reduction in collagen deposition and sustains the improvement in cardiac function. Compelling evidence from animal models and classical in vitro angiogenic approaches demonstrate that a plethora of well-orchestrated signaling pathways involving Notch, Wnt, PI3K, and the modulation of intracellular Ca2+ concentration through ion channels, regulate angiogenesis from existing endothelial cells (ECs) and endothelial progenitor cells (EPCs) in the infarcted heart. Moreover, cardiac repair after MI involves cell-to-cell communication by paracrine/autocrine signals, mainly through the delivery of extracellular vesicles hosting pro-angiogenic proteins and non-coding RNAs, as microRNAs (miRNAs). This review highlights some general insights into signaling pathways activated under MI, focusing on the role of Ca2+ influx, Notch activated pathway, and miRNAs in EC activation and angiogenesis after MI.

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“…There are experiments in which even a cocktail of several molecules is administered, as reported by Du et al (2022), when five small molecules (5SM) are administered to reduce fibrosis in adult MI mice [243]. In recent years, many treatments with different types of cells have been used after cardiac injury in rodent models, i.e., NKx2-5+ cardiac progenitor cells, human mesenchymal stromal cells and endothelial colony forming cells, rat bone marrow stromal cells and hESC-CM [178,[244][245][246]. In this regard, transplantation of hESC-CM for cardiac regeneration is hampered by the formation of fibrotic tissue around the grafts, preventing electrophysiological coupling of CMs [246].…”

Section: Micementioning

confidence: 99%

Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration

Castillo-Casas,

Caño-Carrillo,

Sánchez-Fernández

et al. 2023

JCDD

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Cardiovascular diseases are the leading cause of death worldwide, among which ischemic heart disease is the most representative. Myocardial infarction results from occlusion of a coronary artery, which leads to an insufficient blood supply to the myocardium. As it is well known, the massive loss of cardiomyocytes cannot be solved due the limited regenerative ability of the adult mammalian hearts. In contrast, some lower vertebrate species can regenerate the heart after an injury; their study has disclosed some of the involved cell types, molecular mechanisms and signaling pathways during the regenerative process. In this ‘two parts’ review, we discuss the current state-of-the-art of the main response to achieve heart regeneration, where several processes are involved and essential for cardiac regeneration.

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Combined Transplantation of Human MSCs and ECFCs Improves Cardiac Function and Decrease Cardiomyocyte Apoptosis After Acute Myocardial Infarction

Cited by 9 publications

References 17 publications

Regeneration of the heart: from molecular mechanisms to clinical therapeutics

Regeneration of the heart: from molecular mechanisms to clinical therapeutics

New Insights into the Reparative Angiogenesis after Myocardial Infarction

Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration

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