Log in

Relevant bibliographies by topics / Myocardial infarction. Fibrin. Stem cells / Journal articles

To see the other types of publications on this topic, follow the link: Myocardial infarction. Fibrin. Stem cells.

Journal articles on the topic 'Myocardial infarction. Fibrin. Stem cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Myocardial infarction. Fibrin. Stem cells.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Venugopal, Jayarama Reddy, Molamma P. Prabhakaran, Shayanti Mukherjee, Rajeswari Ravichandran, Kai Dan, and Seeram Ramakrishna. "Biomaterial strategies for alleviation of myocardial infarction." Journal of The Royal Society Interface 9, no. 66 (April 13, 2011): 1–19. http://dx.doi.org/10.1098/rsif.2011.0301.

Full text

Abstract:

World Health Organization estimated that heart failure initiated by coronary artery disease and myocardial infarction (MI) leads to 29 per cent of deaths worldwide. Heart failure is one of the leading causes of death in industrialized countries and is expected to become a global epidemic within the twenty-first century. MI, the main cause of heart failure, leads to a loss of cardiac tissue impairment of left ventricular function. The damaged left ventricle undergoes progressive ‘remodelling’ and chamber dilation, with myocyte slippage and fibroblast proliferation. Repair of diseased myocardium with in vitro -engineered cardiac muscle patch/injectable biopolymers with cells may become a viable option for heart failure patients. These events reflect an apparent lack of effective intrinsic mechanism for myocardial repair and regeneration. Motivated by the desire to develop minimally invasive procedures, the last 10 years observed growing efforts to develop injectable biomaterials with and without cells to treat cardiac failure. Biomaterials evaluated include alginate, fibrin, collagen, chitosan, self-assembling peptides, biopolymers and a range of synthetic hydrogels. The ultimate goal in therapeutic cardiac tissue engineering is to generate biocompatible, non-immunogenic heart muscle with morphological and functional properties similar to natural myocardium to repair MI. This review summarizes the properties of biomaterial substrates having sufficient mechanical stability, which stimulates the native collagen fibril structure for differentiating pluripotent stem cells and mesenchymal stem cells into cardiomyocytes for cardiac tissue engineering.

APA, Harvard, Vancouver, ISO, and other styles

2

Guo, Hai-Dong, Hai-Jie Wang, Yu-Zhen Tan, and Jin-Hong Wu. "Transplantation of Marrow-Derived Cardiac Stem Cells Carried in Fibrin Improves Cardiac Function After Myocardial Infarction." Tissue Engineering Part A 17, no. 1-2 (January 2011): 45–58. http://dx.doi.org/10.1089/ten.tea.2010.0124.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Dyr, Jan E., Tomas Riedel, Jana Stikarova, Jiri Suttnar, Jaroslav Cermak, Roman Kotlin, Martin Hajsl, Petr Tousek, Viktor Kocka, and Martin Maly. "Spatially Organized Structure of Coronary Thrombus in Acute Myocardial Infarction." Blood 128, no. 22 (December 2, 2016): 716. http://dx.doi.org/10.1182/blood.v128.22.716.716.

Full text

Abstract:

Abstract Introduction The use of thromboaspiration in primary percutaneous intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) has offered a unique opportunity to study thrombus composition, its dynamic formation, and architecture in vivo. There has been, however, several limitations, not least the fact that the technique has not yet allowed a precise transversal analysis from one side of the artery to the other, as is done in histological analysis. The dynamic process of intracoronary thrombus formation in STEMI patients is thus still not well understood. Ischemic time was hypothesized to be among the strongest independent correlates of thrombus architecture. In time the platelets are decreasing its proportion and fibrin proportion is increasing (J Silvain, J-P Collet, JW Weisel et al, J Am Coll Cardiol 2011; 57:1359). However, no real report on the internal structures of the in vivo formed thrombi has been shown so far. Therefore, we investigated both the surface and the composition of longitudinally freeze-fractured thrombi. Methods Thrombi were collected by PCI from 119 STEMI patients. Out of the patients there were "early comers " (˃12 h from symptom onset; 23 patients) and "late comers" (more than 720 min; 29 patients). The mean age of all patients was 64 years, 70% of patients were males, 51% were smokers, 50% had arterial hypertension, 20% were diabetics and 23% had chronic renal insufficiency. Scanning electron microscopy; collected thrombi obtained by PCI were thoroughly washed in saline solution and stored in 4% formaldehyde prior dehydration. To reveal the internal structures of the thrombi selected samples were longitudinally freeze fractured in liquid nitrogen and coated with platinum. Samples were examined in SEM Vega Plus TS 5135 (Tescan s.r.o., Brno, Czech Republic). Whole areas of the freeze-fractured thrombi were scanned. Results and discussion The thrombus composition of longitudinally freeze-fractured thrombi was compared between groups of "early-comers" and "late-comers. The distribution of the components in the "early comers" thrombi freeze-fracture seemed to be uniform. Platelets were far the main component (about 75 % in proportion) of the "early comers" thrombus, followed by fibrin and other compounds. The amount of red blood cells was negligible (about 2 - 8 %). We did not observe any significant differences between the thrombi in the group of early comers. Thrombi of the "late-comers" group were composed mainly of red blood cells; platelets and fibrin formed only minority of the thrombi. In contrast to the "early comers" the distribution of the main thrombus components in the "late comers" thrombi was dramatically different between individual parts of the thrombus. The number of platelets and red blood cells varied from 0% to almost 99% and vice versa. It was possible to estimate the initiating place of the thrombus as well as the direction of the growth. Each thrombus could be divided into parts formed mainly either by platelets or by red blood cells. It seems that thrombus develops a regional architecture defined by the extent of platelet activation and packing density. It has been reported that in contracted clots and thrombi, erythrocytes are compressed to close-packed polyhedral structures with platelets and fibrin on the surface demonstrating how contracted clots form an impermeable barrier important for hemostasis and wound healing (D Cines, T Lebedeva, J Weisel et al, Blood 2014; 123:1596). Our investigation of the composition of the in vivo formed thrombi supports these results and helps to explain how fibrinolysis is greatly retarded as clots grow and contract. We have found that on the surfaces of late-comers thrombi fibrin thick fibrils were present. It has been shown that the association of soluble fibrinogen with the fibrin clot results in the reduced adhesiveness of such fibrinogen/fibrin matrices toward leukocytes and platelets (VK Lishko, T Burke, T Ugarova, Blood 2007; 109:1541). Fibrinopeptides A are less accessible for thrombin in surface bound fibrinogen which thus provides additional level of protection of thrombi from premature dissolution (T Riedel, L Medved, JE Dyr, Blood 2011; 117:1700). These findings may have great impact on our knowledge of pathophysiology of the thrombus growth and possible therapeutic consequences related to the time of symptom onset. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

4

Sun, Cheuk-Kwan, Yen-Yi Zhen, Steve Leu, Tzu-Hsien Tsai, Li-Teh Chang, Jiunn-Jye Sheu, Yung-Lung Chen, et al. "Direct implantation versus platelet-rich fibrin-embedded adipose-derived mesenchymal stem cells in treating rat acute myocardial infarction." International Journal of Cardiology 173, no. 3 (May 2014): 410–23. http://dx.doi.org/10.1016/j.ijcard.2014.03.015.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Mattapally, Saidulu, Wuqiang Zhu, Vladimir G. Fast, Ling Gao, Chelsea Worley, Ramaswamy Kannappan, Anton V. Borovjagin, and Jianyi Zhang. "Spheroids of cardiomyocytes derived from human-induced pluripotent stem cells improve recovery from myocardial injury in mice." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (August 1, 2018): H327—H339. http://dx.doi.org/10.1152/ajpheart.00688.2017.

Full text

Abstract:

The microenvironment of native heart tissue may be better replicated when cardiomyocytes are cultured in three-dimensional clusters (i.e., spheroids) than in monolayers or as individual cells. Thus, we differentiated human cardiac lineage-induced pluripotent stem cells in cardiomyocytes (hiPSC-CMs) and allowed them to form spheroids and spheroid fusions that were characterized in vitro and evaluated in mice after experimentally induced myocardial infarction (MI). Synchronized contractions were observed within 24 h of spheroid formation, and optical mapping experiments confirmed the presence of both Ca2+ transients and propagating action potentials. In spheroid fusions, the intraspheroid conduction velocity was 7.0 ± 3.8 cm/s on days 1– 2 after formation, whereas the conduction velocity between spheroids increased significantly ( P = 0.003) from 0.8 ± 1.1 cm/s on days 1– 2 to 3.3 ± 1.4 cm/s on day 7. For the murine MI model, five-spheroid fusions (200,000 hiPSC-CMs/spheroid) were embedded in a fibrin patch and the patch was transplanted over the site of infarction. Later (4 wk), echocardiographic measurements of left ventricular ejection fraction and fractional shortening were significantly greater in patch-treated animals than in animals that recovered without the patch, and the engraftment rate was 25.6% or 30% when evaluated histologically or via bioluminescence imaging, respectively. The exosomes released from the spheroid patch seemed to increase cardiac function. In conclusion, our results established the feasibility of using hiPSC-CM spheroids and spheroid fusions for cardiac tissue engineering, and, when fibrin patches containing hiPSC-CM spheroid fusions were evaluated in a murine MI model, the engraftment rate was much higher than the rates we have achieved via the direct intramyocardial injection. NEW & NOTEWORTHY Spheroids fuse in culture to produce structures with uniformly distributed cells. Furthermore, human cardiac lineage-induced pluripotent stem cells in cardiomyocytes in adjacent fused spheroids became electromechanically coupled as the fusions matured in vitro, and when the spheroids were combined with a biological matrix and administered as a patch over the infarcted region of mouse hearts, the engraftment rate exceeded 25%, and the treatment was associated with significant improvements in cardiac function via a paracrine mechanism, where exosomes released from the spheroid patch.

APA, Harvard, Vancouver, ISO, and other styles

6

Zou, Lili, Hui Liang, LI Hou, Tao Li, Yan Zhang, Baorong LI, Yingmiao LIU, et al. "Neutrophil Extracellular Traps Promote Hypercoagulability in ST-Elevated Myocardial Infarction Following Fibrinolytic Administration." Blood 132, Supplement 1 (November 29, 2018): 3797. http://dx.doi.org/10.1182/blood-2018-99-116105.

Full text

Abstract:

Abstract Introduction:Fibrinolysis plays an important role in the treatment of ST-elevated myocardial infarction (STEMI) when percutaneous coronary intervention is not readily available. Early and successful myocardial reperfusion with thrombolytic therapy effectively reduces the infarct size and improves the clinical outcome. However, the process of restoring blood flow to the ischemic myocardium can induce injury and reduce the beneficial effects of myocardial reperfusion. Previous studies had shown that platelets, leukocytes and TF play important role in thrombotic complications after fibrinolysis in AMI. However, there are still 10-15% patients who have risk for re-occlusion after antiplatelet and anticoagulant therapies. Thus, we speculate that there may be other mechanisms involved in the hypercoagulability after STEMI fibrinolysis. Neutrophil extracellular traps (NETs) are double-edge swords that could ensnare and kill microbial pathogens but also contribute to thrombosis. However, the role of NETs during STEMI fibrinolysis-induced re-occlusion is largely unknown. Our aims were to determine the procoagulant role of NETs after successful thrombolysis, and to elucidate its interaction with endothelial cells (ECs). Methods:31 STEMI patients with successfully fibrinolysis and 12 healthy controls were enrolled. Patient blood samples were collected at 0 h, 2 h, 6 h, 12 h and 24 h after fibrinolysis. Cell-free DNA (cf-DNA) was quantified using the Quant-iT PicoGreen dsDNA Assay Kit. ELISA was used to detect MPO-DNA complexes and TAT (thrombin-antithrombin) complexes. Wright-Giemsa and immunofluorescence confocal microscope were used to analyze and quantify NETs formation in neutrophil cells. ECs were incubated in growth media containing 20% pooled serum obtained from healthy donors in the presence or absence of 20-fold concentrated neutrophil extracellular chromatin. The procoagulant activity (PCA) of neutrophils and ECs was measured by clotting time and purified coagulation complex assays. DNase I or anti-TF were included in the inhibition assays. Results: We found that cf-DNA, MPO-DNA and TAT are significantly reduced at 2 hours in STEMI patients with successful fibrinolysis. Their levels then increased and peaked at 6 hours (Figure 1A, B, E). Interestingly, the level of cf-DNA at 6 hours in STEMI thrombotic patients was positively correlated with TAT (r=0.959; p<0.01; Figure 1G). Wright-Giemsa and immunofluorescence staining showed that NETs were released by STEMI reperfusion neutrophils or by control neutrophils treated with plasma obtained from STEMI patients with fibrinolysis (Figure 1D,F), and the percentage of NETs-releasing PMNs was about 30% (Figure 1C). Isolated neutrophils from fibrinolytic patients in vitro demonstrated significantly shortened coagulation time and increased fibrin formation after 2 hours fibrinolysis, and peaked at 6 hours. DNase I but not anti-tissue factor antibody could inhibit these effects. Co-incubation assays revealed that NETs triggered PS exposure on ECs, converting them to a procoagulant phenotype. Confocal imaging of NETs-treated ECs illustrated that bound FVa and FXa colocalized within PS-enriched areas of ECs to form prothrombinase, and further supported fibrin formation. Moreover, patients with recurrent ischemia showed significantly higher NETs release and thrombin generation than non-recurrent ischemia. Conclusions: Our study reveals that the PCA of STEMI following fibrinolytic administration decrease after 2 hours, then increase and peak at 6 hours, which is at least partly due to the release of NETs induced by activated PMNs. Additionally, NETs partly contribute to ECs injury after myocardial reperfusion. DNase I can disconnect NETs and may therefore serve as a promising therapeutic target in STEMI reinfarction and recurrent ischemia. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

7

Chen, Jiangwei, Yingfei Zhan, Yabin Wang, Dong Han, Bo Tao, Zhenli Luo, Sai Ma, et al. "Chitosan/silk fibroin modified nanofibrous patches with mesenchymal stem cells prevent heart remodeling post-myocardial infarction in rats." Acta Biomaterialia 80 (October 2018): 154–68. http://dx.doi.org/10.1016/j.actbio.2018.09.013.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Chi, Nai-Hsin, Ming-Chia Yang, Tze-Wen Chung, Jia-Yu Chen, Nai-Kuan Chou, and Shoei-Shen Wang. "Cardiac repair achieved by bone marrow mesenchymal stem cells/silk fibroin/hyaluronic acid patches in a rat of myocardial infarction model." Biomaterials 33, no. 22 (August 2012): 5541–51. http://dx.doi.org/10.1016/j.biomaterials.2012.04.030.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Wang, Lei, Jixian Deng, Weichen Tian, Bo Xiang, Tonghua Yang, Gang Li, Jian Wang, et al. "Adipose-derived stem cells are an effective cell candidate for treatment of heart failure: an MR imaging study of rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 3 (September 2009): H1020—H1031. http://dx.doi.org/10.1152/ajpheart.01082.2008.

Full text

Abstract:

This study assessed the potential therapeutic efficacy of adipose-derived stem cells (ASCs) on infarcted hearts. Myocardial infarction was induced in rat hearts by occlusion of the left anterior descending artery (LAD). One week after LAD occlusion, the rats were divided into three groups and subjected to transplantation of ASCs or transplantation of cell culture medium (CCM) or remained untreated. During a 1-mo recovery period, magnetic resonance imaging showed that the ASC-treated hearts had a significantly greater left ventricular (LV) ejection fraction and LV wall thickening than did the CCM-treated and untreated hearts. The capillary density in infarct border zone was significantly higher in the ASC-treated hearts than in the CCM-treated and untreated hearts. However, only 0.5% of the ASCs recovered from the ASC-treated hearts were stained positive for cardiac-specific fibril proteins. It was also found that ASCs under a normal culture condition secreted three cardiac protective growth factors: vascular endothelial growth factor, hepatocyte growth factor, and insulin-like growth factor-1. Results of this study suggest that ASCs were able to improve cardiac function of infarcted rat hearts. Paracrine effect may be the mechanism underlying the improved cardiac function and increased capillary density.

APA, Harvard, Vancouver, ISO, and other styles

10

Weisel, John W., Tatiana Lebedeva, Chandrasekaran Nagaswami, Vincent M. Hayes, Walter Massefski, Rustem I. Litvinov, Lubica Rauova, Thomas J. Lowery, and Douglas B. Cines. "Polyhedrocytes: Compressed Polyhedral Erythrocytes In Contracted Blood Clots and Thrombi." Blood 122, no. 21 (November 15, 2013): 452. http://dx.doi.org/10.1182/blood.v122.21.452.452.

Full text

Abstract:

Background Contraction of blood clots is necessary for hemostasis, wound healing and to restore flow past obstructive thrombi. However, little has been known about the structure of contracted clots and mechanisms of contraction. Erythrocytes, biconcave cells that are highly deformable to allow their passage through the microvasculature, are abundant in venous thrombi, and to a lesser extent in arterial thrombi. Erythrocytes promote hemostasis, but their participation in clot contraction has not been reported. Here we study the mechanisms of clot contraction and the roles of erythrocytes, platelets and fibrin, and show that erythrocyte shape change into compressed polyhedrocytes allows tight packing consistent with the major function of clots to stem bleeding. Methods Whole blood was clotted by recalcification and addition of thrombin or kaolin, while following the process of clotting, including contraction, with a new technique using T2 magnetic resonance. We examined the structure and composition of contracted whole blood clots by scanning electron microscopy and confocal light microscopy. Results Contracted clots display a remarkable structure, with a close-packed, tessellated array (or mosaic tiling of space) of compressed polyhedral erythrocytes (called polyhedrocytes) on the interior and a meshwork of fibrin and platelet aggregates on the exterior. Little fibin and few platelets were found on the interior of the contracted clots. The same results were obtained with both thrombin and kaolin as activators of clotting and also with reconstituted human blood and clots prepared from mouse blood. Confocal microscopy of hydrated clots confirms the results of scanning electron microscopy. The mechanical nature of this shape change was confirmed by polyhedrocyte formation from the forces of centrifugation of blood without clotting. Platelets (with their cytoskeletal motility proteins) and fibrin(ogen) (as the substrate bridging platelets for contraction) are required to generate the forces necessary to segregate platelets/fibrin from erythrocytes and to compress erythrocytes into a closely packed polyhedral array. To assess the density of packing of the polyhedral erythrocytes, we replaced the water surrounding the clots with D2O and observed by T2 magnetic resonance that hydrogen/deuterium exchange for the contracted clots was very slow, consistent with their very tightly packed, almost impermeable structure. The same polyhedrocyte structures were observed from in vivo thrombi aspirated by cardiologists from the coronary arteries of ST-elevation myocardial infarction patients. Summary/Conclusions We have observed a previously undiscovered, naturally occurring erythrocyte function and morphology, closely packed polyhedra, in contracted clots and thrombi, and an unexpected spatial redistribution of platelets and fibrin that occurs during contraction. Clot contraction is an essential part of hemostasis, since both human genetic disorders of platelet myosin IIA and megakaryocyte myosin IIA-knock out mice show a bleeding phenotype. These observations on contracted clots imply that they are stiff, rigid structures that can form an impermeable, watertight seal. On the one hand, contraction of clots within the vasculature may relieve obstruction of blood vessels and allow recanalization, especially in the venous system. On the other hand, these results account for long-standing clinical observations that fibrinolysis is greatly prolonged following clot contraction, since perfusion or diffusion of lytic enzymes into these tightly packed polyhedral erythrocytes would be nearly impossible. These results suggest a vital role for erythrocytes and clot contraction in hemostasis and wound healing. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

11

Chen, Jiangwei, Yingfei Zhan, Yabin Wang, Dong Han, Bo Tao, Zhenli Luo, Sai Ma, et al. "Corrigendum to “Chitosan/silk fibroin modified nanofibrous patches with mesenchymal stem cells prevent heart remodeling post-myocardial infarction in rats” [Acta Biomater. 80 (2018) 154–168]." Acta Biomaterialia 89 (April 2019): 425–26. http://dx.doi.org/10.1016/j.actbio.2019.03.035.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Corinaldesi, Giorgio. "The Ischemic Disease: A Joke Where There's Nothing to Be Gained." Blood 120, no. 21 (November 16, 2012): 5198. http://dx.doi.org/10.1182/blood.v120.21.5198.5198.

Full text

Abstract:

Abstract Abstract 5198 This study explored the hypothesis that the ischemic disease (ID) is associated with systemic alterations of the blood coagulation system: platelet activation (sCD40L: determined by ELISA) and release of various proteins (CRP: determined by nephelometry, IL-6: determined by ELISA). Plasma concentration of these factors were higher in patients with ischemic disease: sCD40L (ID: 724. 2 +/− 58. 4 vs controls 212 +/− 8. 6 pg/ml; p<0001), CRP (ID: 5. 76+/−1. 8 vs controls 2. 54 +/− 0. 3g/l; p<001), IL-6 (ID: 6. 36 +/− 1. 32 vs controls 2. 02 +/− 064 pg/ml; p<001). Platelet activation predicts the risk of ischemic events, in fact CD40L binds and activates alfa IIb/beta 3, and increases PMC (platelet – monocyte complexes), and PDMP (platelet derived microparticle), it also promotes the release of several chemokines (FP4, RANTES, CxCL, ENA 78, NAP-2) that may play an important role in plaque destabilization; high levels of CD40L predict cardiovascular risk of death or myocardial infarction, or stroke within 8 to 12 month in patients with asyntomatic low grade stenosis (carotid or coronary). Several data suggest that CRP has a prognostic value in patients with negative troponin and it is predictive for the development of CAD and refractory ischemic disease, plaque destabilization, and future adverse events, or for the development of severe disease. IL-6 was strongly associated with markers of inflammation (CRP, fibrinogen, white cells count), plasma viscosity, elevated markers of coagulation (fibrin, D-Dimer, FVIII, FIX); moreover IL-6 is associated with insulin resistance, and its levels are high in metabolic syndrome; it is significantly correlated with age, BMI, white cell count; IL-6 increases dendritic platelet forms and acts synergistically with thrombopoietin and stem-cell factor in stimulating megakaryocytopoiesis. Although it has been controversial, IL-6, PCR, and CD40L appear now to be very promising for quantifying the degree of ischemic disease and to monitor or to identify the efficacy and the response to the therapy. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

13

Rao, K. R. S. Sambasiva, KAnanda Krishna, KSai Krishna, Ruben Berrocal, and KS Rao. "Myocardial infarction and stem cells." Journal of Pharmacy and Bioallied Sciences 3, no. 2 (2011): 182. http://dx.doi.org/10.4103/0975-7406.80761.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

McNiece, Ian. "Stem cells for myocardial infarction." Cytotherapy 17, no. 3 (March 2015): 243–44. http://dx.doi.org/10.1016/j.jcyt.2015.01.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Wollert, Kai C., and Helmut Drexler. "Mesenchymal Stem Cells for Myocardial Infarction." Circulation 112, no. 2 (July 12, 2005): 151–53. http://dx.doi.org/10.1161/circulationaha.105.551895.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Limbourg, Florian P., and Helmut Drexler. "Bone Marrow Stem Cells for Myocardial Infarction." Circulation Research 96, no. 1 (January 7, 2005): 6–8. http://dx.doi.org/10.1161/01.res.0000153667.26414.10.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Mazo, Manuel, Juan José Gavira, Beatriz Pelacho, and Felipe Prosper. "Adipose-derived Stem Cells for Myocardial Infarction." Journal of Cardiovascular Translational Research 4, no. 2 (November 30, 2010): 145–53. http://dx.doi.org/10.1007/s12265-010-9246-y.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Siu, Chung-Wah, Song-Yan Liao, Yuan Liu, Qizhou Lian, and Hung-Fat Tse. "Stem cells for myocardial repair." Thrombosis and Haemostasis 104, no. 07 (2010): 6–12. http://dx.doi.org/10.1160/th09-05-0336.

Full text

Abstract:

SummaryThere is a growing interest in the clinical application for stem cell as a novel therapy for treatment of acute myocardial infarction and chronic myocardial ischaemia. The initial premise is the transplanted exogenous stem cells can engraft and integrate with host myocardium for cardiac regeneration. However, recent experimental studies suggest that multiple mechanisms, including remodelling of extracellular matrix, enhancement of neovascularisation and recruitment of endogenous stem cells are more likely to contribute to the beneficial effects of stem cell therapy that direct trans-differentiation of stem cells into functional myocardium. Among different potential cell sources, bone marrow-derived cells and skeletal myoblasts have been tested in pilot clinical trials. Phase I/II randomised controlled clinical trials suggest that intracoronary or intramyocardial injection of bone marrow-derived cells may be safe and feasible strategies for treatment of acute myocardial infarction as well as chronic myocardial ischaemia. In addition, these studies show a modest, but significant improvement in left ventricular ejection fraction and clinical status of patients after cell transplantation. Nevertheless, most of these studies included a relatively small sample size (<200) and short duration of follow-up (<6 months), and the clinical efficacy of stem cell therapy need to be confirmed by future clinical trials. Furthermore, the optimal timing, cell types and mode of delivery need to be addressed, and strategies to improve cell survival and engraftment should also be developed to overcome the potential hurdles related to cell-based therapy.

APA, Harvard, Vancouver, ISO, and other styles

19

Madigan, Mariah, and Rony Atoui. "Therapeutic Use of Stem Cells for Myocardial Infarction." Bioengineering 5, no. 2 (April 6, 2018): 28. http://dx.doi.org/10.3390/bioengineering5020028.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Ko, Il-Kwon, and Byung-Soo Kim. "Mesenchymal Stem Cells for Treatment of Myocardial Infarction." International Journal of Stem Cells 1, no. 1 (November 30, 2008): 49–54. http://dx.doi.org/10.15283/ijsc.2008.1.1.49.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Docshin, P. M., A. A. Karpov, Sh D. Eyvazova, M. V. Puzanov, A. A. Kostareva, M. M. Galagudza, and A. B. Malashicheva. "ACTIVATION OF CARDIAC STEM CELLS IN MYOCARDIAL INFARCTION." Tsitologiya 60, no. 2 (2018): 81–88. http://dx.doi.org/10.31116/tsitol.2018.02.02.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Mills, James S., and Sunil V. Rao. "REPAIR-AMI: stem cells for acute myocardial infarction." Future Cardiology 3, no. 2 (March 2007): 137–40. http://dx.doi.org/10.2217/14796678.3.2.137.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Oh, Jaewon, Hyunseok Kang, Ji Hyung Chung, and Yangsoo Jang. "Autologous bone-marrow stem cells for myocardial infarction." Lancet 368, no. 9529 (July 2006): 27. http://dx.doi.org/10.1016/s0140-6736(06)68963-0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Docshin, P. M., A. A. Karpov, Sh D. Eyvazova, M. V. Puzanov, A. A. Kostareva, M. M. Galagudza, and A. B. Malashicheva. "Activation of Cardiac Stem Cells in Myocardial Infarction." Cell and Tissue Biology 12, no. 3 (May 2018): 175–82. http://dx.doi.org/10.1134/s1990519x18030045.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Beitnes, Jan Otto, Ketil Lunde, Jan E. Brinchmann, and Svend Aakhus. "Stem cells for cardiac repair in acute myocardial infarction." Expert Review of Cardiovascular Therapy 9, no. 8 (August 2011): 1015–25. http://dx.doi.org/10.1586/erc.11.108.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Dutta, Partha, Hendrik B. Sager, Kristy R. Stengel, Kamila Naxerova, Gabriel Courties, Borja Saez, Lev Silberstein, et al. "Myocardial Infarction Activates CCR2+ Hematopoietic Stem and Progenitor Cells." Cell Stem Cell 16, no. 5 (May 2015): 477–87. http://dx.doi.org/10.1016/j.stem.2015.04.008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Mollmann, H., H. Nef, A. Elsasser, and C. Hamm. "Stem cells in myocardial infarction: from bench to bedside." Heart 95, no. 6 (February 27, 2009): 508–14. http://dx.doi.org/10.1136/hrt.2007.125054.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Lalit, Pratik A., Derek J. Hei, Amish N. Raval, and Timothy J. Kamp. "Induced Pluripotent Stem Cells for Post–Myocardial Infarction Repair." Circulation Research 114, no. 8 (April 11, 2014): 1328–45. http://dx.doi.org/10.1161/circresaha.114.300556.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Liang, Simon X., and William D. Phillips. "Migration of Resident Cardiac Stem Cells in Myocardial Infarction." Anatomical Record 296, no. 2 (December 5, 2012): 184–91. http://dx.doi.org/10.1002/ar.22633.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Hou, Jingying, Lingyun Wang, Jieyu Jiang, Changqing Zhou, Tianzhu Guo, Shaoxin Zheng, and Tong Wang. "Cardiac Stem Cells and their Roles in Myocardial Infarction." Stem Cell Reviews and Reports 9, no. 3 (December 13, 2012): 326–38. http://dx.doi.org/10.1007/s12015-012-9421-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

31

Raziyeva, Kamila, Aiganym Smagulova, Yevgeniy Kim, Saltanat Smagul, Ayan Nurkesh, and Arman Saparov. "Preconditioned and Genetically Modified Stem Cells for Myocardial Infarction Treatment." International Journal of Molecular Sciences 21, no. 19 (October 2, 2020): 7301. http://dx.doi.org/10.3390/ijms21197301.

Full text

Abstract:

Ischemic heart disease and myocardial infarction remain leading causes of mortality worldwide. Existing myocardial infarction treatments are incapable of fully repairing and regenerating the infarcted myocardium. Stem cell transplantation therapy has demonstrated promising results in improving heart function following myocardial infarction. However, poor cell survival and low engraftment at the harsh and hostile environment at the site of infarction limit the regeneration potential of stem cells. Preconditioning with various physical and chemical factors, as well as genetic modification and cellular reprogramming, are strategies that could potentially optimize stem cell transplantation therapy for clinical application. In this review, we discuss the most up-to-date findings related to utilizing preconditioned stem cells for myocardial infarction treatment, focusing mainly on preconditioning with hypoxia, growth factors, drugs, and biological agents. Furthermore, genetic manipulations on stem cells, such as the overexpression of specific proteins, regulation of microRNAs, and cellular reprogramming to improve their efficiency in myocardial infarction treatment, are discussed as well.

APA, Harvard, Vancouver, ISO, and other styles

32

Carvalho, Juliana L., Vinicius B. A. Braga, Marcos B. Melo, Ana Carolina D. A. Campos, Maira S. Oliveira, Dawidson A. Gomes, Anderson J. Ferreira, Robson A. S. Santos, and Alfredo M. Goes. "Priming mesenchymal stem cells boosts stem cell therapy to treat myocardial infarction." Journal of Cellular and Molecular Medicine 17, no. 5 (March 14, 2013): 617–25. http://dx.doi.org/10.1111/jcmm.12036.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Berry, Mark F., Adam J. Engler, Y. Joseph Woo, Timothy J. Pirolli, Lawrence T. Bish, Vasant Jayasankar, Kevin J. Morine, Timothy J. Gardner, Dennis E. Discher, and H. Lee Sweeney. "Mesenchymal stem cell injection after myocardial infarction improves myocardial compliance." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 6 (June 2006): H2196—H2203. http://dx.doi.org/10.1152/ajpheart.01017.2005.

Full text

Abstract:

Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSCs) into the acutely ischemic myocardium. Two weeks postinfarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were twofold stiffer than myocardium from noninfarcted animals but softer than myocardium from vehicle-treated infarcted animals. After 8 wk, the following variables were evaluated: MSC engraftment and left ventricular geometry by histological methods, cardiac function with a pressure-volume conductance catheter, myocardial fibrosis by Masson Trichrome staining, vascularity by immunohistochemistry, and apoptosis by TdT-mediated dUTP nick-end labeling assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated postinfarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.

APA, Harvard, Vancouver, ISO, and other styles

34

Yan, Weiang, Ejlal Abu-El-Rub, Sekaran Saravanan, Lorrie A. Kirshenbaum, Rakesh C. Arora, and Sanjiv Dhingra. "Inflammation in myocardial injury: mesenchymal stem cells as potential immunomodulators." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 2 (August 1, 2019): H213—H225. http://dx.doi.org/10.1152/ajpheart.00065.2019.

Full text

Abstract:

Ischemic heart disease is a growing worldwide epidemic. Improvements in medical and surgical therapies have reduced early mortality after acute myocardial infarction and increased the number of patients living with chronic heart failure. The irreversible loss of functional cardiomyocytes puts these patients at significant risk of ongoing morbidity and mortality after their index event. Recent evidence suggests that inflammation is a key mediator of postinfarction adverse remodeling in the heart. In this review, we discuss the cardioprotective and deleterious effects of inflammation and its mediators during acute myocardial infarction. We also explore the role of mesenchymal stem cell therapy to limit secondary injury and promote myocardial healing after myocardial infarction.

APA, Harvard, Vancouver, ISO, and other styles

35

Copeland, Nathan, David Harris, and Mohamed A. Gaballa. "Human umbilical cord blood stem cells, myocardial infarction and stroke." Clinical Medicine 9, no. 4 (August 2009): 342–45. http://dx.doi.org/10.7861/clinmedicine.9-4-342.

Full text

APA, Harvard, Vancouver, ISO, and other styles

36

Rodriguez-Losada, Noela, Manuel F. Jimenez-Navarro, Borja Fernandez, Carmen Rueda-Martinez, Antonia Aranega, Juan A. Marchal, and Eduardo de Teresa Galvan. "Resident and Non-Resident Stem Cells in Acute Myocardial Infarction." Cardiovascular & Hematological Disorders-Drug Targets 10, no. 3 (September 1, 2010): 202–15. http://dx.doi.org/10.2174/1871529x11006030202.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Shafiq, Muhammad, Sang-Hoon Lee, Youngmee Jung, and Soo Kim. "Strategies for Recruitment of Stem Cells to Treat Myocardial Infarction." Current Pharmaceutical Design 21, no. 12 (February 20, 2015): 1584–97. http://dx.doi.org/10.2174/1381612821666150115151938.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Chen, Zhi, Long Chen, Chunyu Zeng, and Wei Eric Wang. "Functionally Improved Mesenchymal Stem Cells to Better Treat Myocardial Infarction." Stem Cells International 2018 (November 25, 2018): 1–14. http://dx.doi.org/10.1155/2018/7045245.

Full text

Abstract:

Myocardial infarction (MI) is one of the leading causes of death worldwide. Mesenchymal stem cell (MSC) transplantation is considered a promising approach and has made significant progress in preclinical studies and clinical trials for treating MI. However, hurdles including poor survival, retention, homing, and differentiation capacity largely limit the therapeutic effect of transplanted MSCs. Many strategies such as preconditioning, genetic modification, cotransplantation with bioactive factors, and tissue engineering were developed to improve the survival and function of MSCs. On the other hand, optimizing the hostile transplantation microenvironment of the host myocardium is also of importance. Here, we review the modifications of MSCs as well as the host myocardium to improve the efficacy of MSC-based therapy against MI.

APA, Harvard, Vancouver, ISO, and other styles

39

Thoelen, M. "Ultrastructure of transplanted mesenchymal stem cells after acute myocardial infarction." Heart 90, no. 9 (September 1, 2004): 1046. http://dx.doi.org/10.1136/hrt.2003.032193.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Li, Zicheng, Jun Guo, Qing Chang, and Aidong Zhang. "Paracrine Role for Mesenchymal Stem Cells in Acute Myocardial Infarction." Biological & Pharmaceutical Bulletin 32, no. 8 (2009): 1343–46. http://dx.doi.org/10.1248/bpb.32.1343.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Singh, Sarabjeet, Rohit Arora, Kamna Handa, Ahmad Khraisat, Nagapradeep Nagajothi, Janos Molnar, and Sandeep Khosla. "Stem Cells Improve Left Ventricular Function in Acute Myocardial Infarction." Clinical Cardiology 32, no. 4 (April 2009): 176–80. http://dx.doi.org/10.1002/clc.20470.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Sharif, Faisal, Jozef Bartunek, and Marc Vanderheyden. "Adult stem cells in the treatment of acute myocardial infarction." Catheterization and Cardiovascular Interventions 77, no. 1 (December 22, 2010): 72–83. http://dx.doi.org/10.1002/ccd.22620.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Miyahara, Yoshinori, Noritoshi Nagaya, Masaharu Kataoka, Bobby Yanagawa, Koichi Tanaka, Hiroyuki Hao, Kozo Ishino, et al. "Monolayered mesenchymal stem cells repair scarred myocardium after myocardial infarction." Nature Medicine 12, no. 4 (April 2006): 459–65. http://dx.doi.org/10.1038/nm1391.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Ventura, C. "Stem Cells for Repairing Myocardial Infarction and Improving Heart Failure." Biomedicine & Pharmacotherapy 62, no. 8 (October 2008): 496–97. http://dx.doi.org/10.1016/j.biopha.2008.07.019.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Bollini, Sveva, King K. Cheung, Johannes Riegler, Xuebin Dong, Nicola Smart, Marco Ghionzoli, Stavros P. Loukogeorgakis, et al. "Amniotic Fluid Stem Cells Are Cardioprotective Following Acute Myocardial Infarction." Stem Cells and Development 20, no. 11 (November 2011): 1985–94. http://dx.doi.org/10.1089/scd.2010.0424.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Carbone, R. G., A. Monselise, G. Bottino, S. Negrini, and F. Puppo. "Stem cells therapy in acute myocardial infarction: a new era?" Clinical and Experimental Medicine 21, no. 2 (January 23, 2021): 231–37. http://dx.doi.org/10.1007/s10238-021-00682-3.

Full text

Abstract:

AbstractStem cells transplantation after acute myocardial infarction (AMI) has been claimed to restore cardiac function. However, this therapy is still restricted to experimental studies and clinical trials. Early un-blinded studies suggested a benefit from stem cell therapy following AMI. More recent blinded randomized trials have produced mixed results and, notably, the last largest pan-European clinical trial showed the inconclusive results. Furthermore, mechanisms of potential benefit remain uncertain. This review analytically evaluates 34 blinded and un-blinded clinical trials comprising 3142 patients and is aimed to: (1) identify the pros and cons of stem cell therapy up to a 6-month follow-up after AMI comparing benefit or no effectiveness reported in clinical trials; (2) provide useful information for planning future clinical programs of cardiac stem cell therapy.

APA, Harvard, Vancouver, ISO, and other styles

47

Leri, Annarosa, Jan Kajstura, and Piero Anversa. "Cardiac Stem Cells and Mechanisms of Myocardial Regeneration." Physiological Reviews 85, no. 4 (October 2005): 1373–416. http://dx.doi.org/10.1152/physrev.00013.2005.

Full text

Abstract:

This review discusses current understanding of the role that endogenous and exogenous progenitor cells may have in the treatment of the diseased heart. In the last several years, a major effort has been made in an attempt to identify immature cells capable of differentiating into cell lineages different from the organ of origin to be employed for the regeneration of the damaged heart. Embryonic stem cells (ESCs) and bone marrow-derived cells (BMCs) have been extensively studied and characterized, and dramatic advances have been made in the clinical application of BMCs in heart failure of ischemic and nonischemic origin. However, a controversy exists concerning the ability of BMCs to acquire cardiac cell lineages and reconstitute the myocardium lost after infarction. The recognition that the adult heart possesses a stem cell compartment that can regenerate myocytes and coronary vessels has raised the unique possibility to rebuild dead myocardium after infarction, to repopulate the hypertrophic decompensated heart with new better functioning myocytes and vascular structures, and, perhaps, to reverse ventricular dilation and wall thinning. Cardiac stem cells may become the most important cell for cardiac repair.

APA, Harvard, Vancouver, ISO, and other styles

48

Jiang, Zhi, and Jian an Wang. "MENSTRUAL BLOOD STEM CELLS IMPROVED MYOCARDIAL SURVIVAL AFTER RAT MYOCARDIAL INFARCTION BY PARACRINE." Heart 98, Suppl 2 (October 2012): E170.2—E170. http://dx.doi.org/10.1136/heartjnl-2012-302920j.31.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

Zafiriou, Maria Patapia, Claudia Noack, Bernhard Unsöld, Michael Didie, Elena Pavlova, Henrike J. Fischer, Holger M. Reichardt, et al. "Erythropoietin Responsive Cardiomyogenic Cells Contribute to Heart Repair Post Myocardial Infarction." STEM CELLS 32, no. 9 (August 18, 2014): 2480–91. http://dx.doi.org/10.1002/stem.1741.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Ling, Lin, Shaohua Gu, and Yan Cheng. "Resveratrol activates endogenous cardiac stem cells and improves myocardial regeneration following acute myocardial infarction." Molecular Medicine Reports 15, no. 3 (January 25, 2017): 1188–94. http://dx.doi.org/10.3892/mmr.2017.6143.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!