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31.
F. van den Akker J.C. Deddens P.A. Doevendans J.P.G. Sluijter 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
After myocardial infarction (MI) a local inflammatory reaction clears the damaged myocardium from dead cells and matrix debris at the onset of scar formation. The intensity and duration of this inflammatory reaction are intimately linked to post-infarct remodeling and cardiac dysfunction. Strikingly, treatment with standard anti-inflammatory drugs worsens clinical outcome, suggesting a dual role of inflammation in the cardiac response to injury. Cardiac stem cell therapy with different stem or progenitor cells, e.g. mesenchymal stem cells (MSC), was recently found to have beneficial effects, mostly related to paracrine actions. One of the suggested paracrine effects of cell therapy is modulation of the immune system.Scope of review
MSC are reported to interact with several cells of the immune system and could therefore be an excellent means to reduce detrimental inflammatory reactions and promote the switch to the healing phase upon cardiac injury. This review focuses on the potential use of MSC therapy for post-MI inflammation. To understand the effects MSC might have on the post-MI heart the cellular and molecular changes in the myocardium after MI need to be understood.Major conclusions
By studying the general pathways involved in immunomodulation, and examining the interactions with cell types important for post-MI inflammation, it becomes clear that MSC treatment might provide a new therapeutic opportunity to improve cardiac outcome after acute injury.General significance
Using stem cells to target the post-MI inflammation is a novel therapy which could have considerable clinical implications. This article is part of a Special Issue entitled Biochemistry of Stem Cells. 相似文献32.
Gathier W. A. Salden O. A. E. van Ginkel D. J. van Everdingen W. M. Mohamed Hoesein F. A. A. Cramer M. J. M. Doevendans P. A. Meine M. Chamuleau S. A. J. van Slochteren F. J. 《Netherlands heart journal》2020,28(2):89-95
Netherlands Heart Journal - To determine the feasibility and potential benefit of a full cardiac magnetic resonance (CMR) work-up for assessing the location of scarred myocardium and the... 相似文献
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Fatih Arslan Ruenn Chai Lai Mirjam B. Smeets Lars Akeroyd Andre Choo Eissa N.E. Aguor Leo Timmers Harold V. van Rijen Pieter A. Doevendans Gerard Pasterkamp Sai Kiang Lim Dominique P. de Kleijn 《Stem cell research》2013,10(3):301-312
We have previously identified exosomes as the paracrine factor secreted by mesenchymal stem cells. Recently, we found that the key features of reperfusion injury, namely loss of ATP/NADH, increased oxidative stress and cell death were underpinned by proteomic deficiencies in ischemic/reperfused myocardium, and could be ameliorated by proteins in exosomes. To test this hypothesis in vivo, mice (C57Bl6/J) underwent 30 min ischemia, followed by reperfusion (I/R injury). Purified exosomes or saline was administered 5 min before reperfusion. Exosomes reduced infarct size by 45% compared to saline treatment. Langendorff experiments revealed that intact but not lysed exosomes enhanced viability of the ischemic/reperfused myocardium. Exosome treated animals exhibited significant preservation of left ventricular geometry and contractile performance during 28 days follow-up. Within an hour after reperfusion, exosome treatment increased levels of ATP and NADH, decreased oxidative stress, increased phosphorylated-Akt and phosphorylated-GSK-3β, and reduced phosphorylated-c-JNK in ischemic/reperfused hearts. Subsequently, both local and systemic inflammation were significantly reduced 24 h after reperfusion. In conclusion, our study shows that intact exosomes restore bioenergetics, reduce oxidative stress and activate pro-survival signaling, thereby enhancing cardiac function and geometry after myocardial I/R injury. Hence, mesenchymal stem cell-derived exosomes are a potential adjuvant to reperfusion therapy for myocardial infarction. 相似文献
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Repair of diseased or injured myocardium by cell-based therapies is likely to require a multi-pronged approach. New myocytes will need to be generated, integrated with existing myocardial tissue, and perfused with a newly acquired vascular system. There are many potential avenues to achieve this goal, and optimizing repair is likely to require a synthetic therapeutic approach. In this review, we discuss several issues to be considered in cell-based cardiac repair, some progress which has been made toward this goal, and future directions. 相似文献
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van Spaendonck-Zwarts KY van der Kooi AJ van den Berg MP Ippel EF Boven LG Yee WC van den Wijngaard A Brusse E Hoogendijk JE Doevendans PA de Visser M Jongbloed JD van Tintelen JP 《Netherlands heart journal》2012,20(5):219-228
Background
Desmin-related myopathy (DRM) is an autosomally inherited skeletal and cardiac myopathy, mainly caused by dominant mutations in the desmin gene (DES). We describe new families carrying the p.S13F or p.N342D DES mutations, the cardiac phenotype of all carriers, and the founder effects.Methods
We collected the clinical details of all carriers of p.S13F or p.N342D. The founder effects were studied using genealogy and haplotype analysis.Results
We identified three new index patients carrying the p.S13F mutation and two new families carrying the p.N342D mutation. In total, we summarised the clinical details of 39 p.S13F carriers (eight index patients) and of 21 p.N342D carriers (three index patients). The cardiac phenotype of p.S13F carriers is fully penetrant and severe, characterised by cardiac conduction disease and cardiomyopathy, often with right ventricular involvement. Although muscle weakness is a prominent and presenting symptom in p.N342D carriers, their cardiac phenotype is similar to that of p.S13F carriers. The founder effects of p.S13F and p.N342D were demonstrated by genealogy and haplotype analysis.Conclusion
DRM may occur as an apparently isolated cardiological disorder. The cardiac phenotypes of the DES founder mutations p.S13F and p.N342D are characterised by cardiac conduction disease and cardiomyopathy, often with right ventricular involvement.Electronic supplementary material
The online version of this article (doi:10.1007/s12471-011-0233-y) contains supplementary material, which is available to authorized users. 相似文献37.
Tietge WJ de Heer LM van Hessen MW Jansen R Bots ML van Gilst W Schalij M Klautz RJ Van den Brink RB Van Herwerden LA Doevendans PA Chamuleau SA Kluin J 《Netherlands heart journal》2012,20(3):94-101
Background
Asymptomatic severe mitral valve (MV) regurgitation with preserved left ventricular function is a challenging clinical entity as data on the recommended treatment strategy for these patients are scarce and conflicting. For asymptomatic patients, no randomised trial has been performed for objectivising the best treatment strategy.Methods
The Dutch AMR (Asymptomatic Mitral Regurgitation) trial is a multicenter, prospective, randomised trial comparing early MV repair versus watchful waiting in asymptomatic patients with severe organic MV regurgitation. A total of 250 asymptomatic patients (18–70 years) with preserved left ventricular function will be included. Intervention will be either watchful waiting or MV surgery. Follow-up will be 5 years. Primary outcome measures are all-cause mortality and a composite endpoint of cardiovascular mortality, congestive heart failure, and hospitalisation for non-fatal cardiovascular and cerebrovascular events. Secondary outcome measures are total costs, cost-effectiveness, quality of life, echocardiographic and cardiac magnetic resonance parameters, exercise tests, asymptomatic atrial fibrillation and brain natriuretic peptide levels. Additionally, the complication rate in the surgery group and rate of surgery in the watchful waiting group will be determined.Implications
The Dutch AMR trial will be the first multicenter randomised trial on this topic. We anticipate that the results of this study are highly needed to elucidate the best treatment strategy and that this may prove to be an international landmark study. 相似文献38.
Tycho I.G. van der Spoel Krijn R. Vrijsen Stefan Koudstaal Joost P.G. Sluijter Johannes Frank W. Nijsen Hugo W. de Jong Imo E. Hoefer Maarten‐Jan M. Cramer Pieter A. Doevendans Eric van Belle Steven A.J. Chamuleau 《Journal of cellular and molecular medicine》2012,16(11):2768-2776
Stem cell therapy is a new strategy for chronic ischaemic heart disease in patients. However, no consensus exists on the most optimal delivery strategy. This randomized study was designed to assess cell delivery efficiency of three clinically relevant strategies: intracoronary (IC) and transendocardial (TE) using electromechanical mapping guidance (NOGA) compared to surgical delivery in a chronic pig model of ischaemic cardiomyopathy. Twenty‐four animals underwent delivery of 107 autologous Indium‐oxine‐labelled bone marrow‐derived mesenchymal stem cells (MSC) 4 weeks after infarction and were randomized to one of three groups (n = 8 each group): IC, TE or surgical delivery (reference group). Primary endpoint was defined as percentage (%) of injected dose per organ and assessed by in vivo gamma‐emission counting. In addition, troponin and coronary flow were assessed before and after MSC injection. Blinded endpoint analysis showed no significant difference in efficiency after surgical (16 ± 4%), IC (11 ± 1%) and TE (11 ± 3%) (P = 0.52) injections. IC showed less variability in efficiency compared with TE and surgical injection. Overall, TE injection showed less distribution of MSC to visceral organs compared with other modalities. Troponin rise and IC flow did not differ between the percutaneous groups. This randomized study showed no significant difference in cell delivery efficiency to the myocardium in a clinically relevant ischaemic large animal model between IC and TE delivery. In addition, no differences in safety profile were observed. These results are important in view of the choice of percutaneous cell delivery modality in future clinical stem cell trials. 相似文献
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Jeroen Slikkerveer Pieter A Dijkmans Gertjan T Sieswerda Pieter AFM Doevendans Arie PJ van Dijk Freek WA Verheugt Thomas R Porter Otto Kamp 《Trials》2008,9(1):1-7