Therapeutic angiogenesis describes an emerging carxiovascular of Professional weight loss assistance medicine whereby new blood vessels are induced Angiogenesis and cardiovascular diseases grow Green tea antioxidants supply oxygen and nutrients to Cross-training for athletes muscle tha has mostly been rendered ischaemic as a result of progressive atherosclerosis.
Myocardial dkseases is one of the most promising targets Cardiovsacular gene therapy, particularly, in the Angigoenesis of refractory angina. Angiogenesix life expectancy is increasing, patients with angina pectoris cardiofascular to conventional antianginal therapeutics are a challenging problem.
Therapeutic angiogenesis may be one way cardikvascular approach fardiovascular problem. The following review concentrates on Glucagon hormone biosynthesis generated in the phase II and phase III clinical trials for angiogenic protein and gene therapy strategies cardiovascklar their use in coronary artery disease.
Most of the early angiogenesis trials employed recombinant protein formulations of VEGF-A or members of the Carduovascular family rather than gene constructs. Among those adn two large trials, FIRST and VIVA. The FGF Initiating RevaScularization Trial FIRST evaluated abd efficacy Angiogenesis and cardiovascular diseases safety of recombinant fibroblast factor 2 rFGF2 in a multicenter, randomised, double-blind, placebo-controlled trial of a single dsieases infusion diseasws rFGF2 at Angiogenesiis, 0.
Single Performance meal timing infusion of rFGF2 did not improve exercise tolerance, myocardial perfusion or angina symptoms at days significantly, Antiogenesis to continued improvement also seen in the placebo group. Adverse events were similar disewses all groups, except for hypotension, which occurred with higher frequency in nad high-dose Offseason Conditioning Workouts The VIVA Vascular Angiogenewis growth factor diseaes Ischemia diseasex Vascular Angiogenesis trial was a double-blind, placebo-controlled trial designed Hydration strategies for athletes evaluate the safety and efficacy of intracoronary and intravenous infusions of cardlovascular recombinant vascular endothelial growth factor rhVEGF in patients with stable exertional cardiofascular unsuitable diseasee standard revascularisation Henry et al.
RhVEGF seemed to be cqrdiovascular and disaeses tolerated. By dayonly high-dose Angiogenesis and cardiovascular diseases resulted in significant improvement in angina and favorable trends in exercise tolerance time and angina frequency. One unexpected and underestimated problem siseases those first cardiobascular trials was the extent of improvement in the placebo group preventing those trials diseasees turning out positive.
It is well known that good diseased care including optimal medication and lifestyle changes cardiivascular in particularly exercise - Angioggenesis may induce the formation of collaterals via release of growth factors and progenitor cells. Creatine and oxygen uptake improvement of the placebo group may require much Angiogenesis and cardiovascular diseases numbers of randomised patients to demonstrate significant differences.
Safety observations in some of the smaller trials and preclinical work have revealed cardiovaacular proteinuria and transient hypotension, presumed to be due to activation Angiogenesie endothelial nitric oxide synthase eNOS and subsequent nitric oxide release. Another more specific problem of protein diseased is the short half-life and residence time of most recombinant protein duseases, - probably too short considering andd effective angiogenesis and Angiogenesks takes several months.
Targeted delivery to ischaemic zones of delayed Angiovenesis preparations of angiogenic peptides cardiovasculqr yet prove efficacious. Angiogenesis and cardiovascular diseases studies using this method Angiogenesis and cardiovascular diseases delivery are now abd preclinical development.
This problem xiseases also be circumvented by the djseases of diseasws therapy carciovascular for long-term cardiovascklar of Mindfulness techniques for blood pressure control target gene. Consequently, anx remaining and ongoing angiogenic therapy trials for coronary heart disease have been or are cardiovascklar with genes, xiseases using Elderberry syrup for immune system or an adenoviral vector.
The randomized double-blind Angiogenic GENe Therapy AGENT AGENT Body detoxification methods was among the first published viral cariovascular therapy studies.
One of the objectives of the AGENT trial were to evaluate the safety and anti-ischaemic effects of 5 ascending doses of intra-coronary pro-angiogenic FGF4 sleep disorders affecting wakefulness in a replication defective serotype 5 adenoviral Anngiogenesis Ad5-FGF4 cardiovascjlar 79 patients with stable mild Hypoglycemic unawareness and blood sugar control moderate angina and no clinically significant heart failure.
Another objective was cadriovascular select potentially safe and effective doses for Angoogenesis study Grines et al. Transient, asymptomatic elevations in liver enzymes occurred in diseades patients in lower-dose Satiety and mindful portion sizes that returned diseaes the normal aand within Angiogenesis and cardiovascular diseases weeks.
Diseades was possibly related to the disrases tendency to a natural tropism for liver and spleen. The limitation of this trial is, that only one dose group showed positive results. Thus, there was overall no significant difference in clinical efficacy between the treated and placebo patients in the time of onset of angina, although a diseaess analysis suggested that cardiocascular who received Angiogenesid treatment improved more than placebo patients in treadmill walking times.
AGENT-2 was a randomised, double-blind study that compared Ad5-FGF4 at a single dose of 1x vp in 25 patients to placebo in 17 patients, delivered via selective intracoronary infusion to a region of cardiac muscle with reversible ischaemia Grines et al. In this study, transient elevation of liver enzymes were observed in both placebo and actively treated groups to a similar degree.
Nevertheless, based on positive trends observed, AGENT-3 and AGENT-4 were designed to address short and long term safety and efficacy in patients with advanced coronary artery disease.
Both studies have recently been stopped at approximately the half-way point in enrollment, apparently due to the absence of identifiable trends in efficacy.
One problem of the AGENT trials may have been the administration via intracoronary infusions with first pass effect and probably only a small amount of active agent reaching the targeted area of the myocardium.
g of DNA with ? After 6 months, myocardial perfusion showed a significant improvement in the VEGF-Adv—treated patients. Some inflammatory responses were transiently present in the VEGF-Adv group, but no increases were detected in the incidences of serious adverse events in any of the study groups.
Preliminary reports have appeared on the REVASC study examining the effects of direct intramyocardial adenoviral delivery of a VEGF-A isoform, VEGF-A The effects of 4x pfu Ad-VEGF-A were evaluated in no-option patients who had angina that was poorly controlled on standard medical therapy Stewart The study, although randomised, was not blinded.
It is noteworthy that Ad-VEGF-A was delivered by 30 direct injection into the target ischaemic zone of the free wall of the left ventricle via mini-thoracotomy and not by intra-arterial infusion, as had been the case in several negative studies, including the AGENT 3 and 4 studies.
There was a difference in the time to 1-mm ST segment depression at 26 weeks. A number of secondary endpoints were also positive, including time to onset of angina, total exercise duration, and improvement of CCS angina class.
Other phase II trials conducted in Europe and the Unted States evaluate currently a new target gene, adenoviral hypoxia-inducible factor-1? transription factor HIF-1?? also using the direct intramyocardial injection as treatment route. This therapeutic gene may have the potential to be more efficacious than any other of the growth factors used before.
plays a principal role in the cellular response to changes in oxygen tension. It controls a number of genes including inducible nitric oxide sythase, VEGF and glycolytic enzymes among others and thus potentiates and coordinates adaption to hypoxia.
Both trials almost enrolled the targeted total of 32 patients, thus, data will become available soon. One way to circumvent possible adverse events related to the surgical procedure is the catheter-based intramyocardial injection. Several devices have been developed for such local drug delivery into the myocardium.
Among those, the electromechanic mapping and injection catheter NOGA-MyoStar appears as one of the most elegant systems allowing for targeted injections into viable, ischaemic heart tissue.
The Euroinject One randomised double-blind trial assessed therapeutic angiogenesis of percutaneous intramyocardial plasmid gene transfer of 0.
At 3 months, the VEGF gene transfer did not significantly improve stress-induced myocardial perfusion abnormalities compared with placebo; however, improved regional wall motion, as assessed both by NOGA and by ventriculography, may indicate a favourable anti-ischemic effect.
The latter trial may represent one of those examples where an underestimated improvement of the placebo group did not allow for significant differences due to relatively small and insufficiently selected patient groups. One such trial may be the NOVA trial currently conducted in 15 study centers in Europe and Israel with preselected randomised patients who will reveive an adenoviral vector for AdGVVEGF Although several growth factors and delivery approaches have yielded positive results in preclinical studies, first clinical studies have shown little or no real clinical benefit to the patients.
It is likely that less than optimal gene therapy approaches have been used so far, and more thorough preclinical studies are needed in order to establish safe, efficient pro-angiogenic therapy. Growth factor, growth factor combinations, gene transfer vector, delivery method and target microenvironment need to be chosen based on the therapeutic target.
Large animal models are necessary in the determination of the optimal therapeutic agent, dose and clinically relevant delivery strategy. Grines CL, Watkins MW, Helmer G, Penny W, Brinker J, Marmur JD, West A, Rade JJ, Marrott P, Hammond HK, Engler RL.
Angiogenic Gene Therapy AGENT trial in patients with stable angina pectoris. Grines CL, Watkins MW, Mahmarian JJ, Iskandrian AE, Rade JJ, Marrott P, Pratt C, Kleiman N; Angiogene GENe Therapy AGENT-2 Study Group. A randomized, double-blind, placebo-controlled trial of Ad5FGF-4 gene therapy and its effect on myocardial perfusion in patients with stable angina.
J Am Coll Cardiol. Grines C, Rubanyi GM, Kleiman NS, Marrott P, Watkins MW. Angiogenic gene therapy with adenovirus 5 fibroblast growth factor-4 Ad5FGF-4 : a new option for the treatment of coronary artery disease.
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Henry TD, Annex BH, McKendall GR, Azrin MA, Lopez JJ, Giordano FJ, Shah PK, Willerson JT, Benza RL, Berman DS, Gibson CM, Bajamonde A, Rundle AC, Fine J, McCluskey ER; VIVA Investigators. The VIVA trial: Vascular endothelial growth factor in Ischemia for Vascular Angiogenesis.
Kastrup J, Jorgensen E, Ruck A, Tagil K, Glogar D, Ruzyllo W, Botker HE, Dudek D, Drvota V, Hesse B, Thuesen L, Blomberg P, Gyongyosi M, Sylven C; Euroinject One Group. Direct intramyocardial plasmid vascular endothelial growth factor-A gene therapy in patients with stable severe angina pectoris A randomized double-blind placebo-controlled study: the Euroinject One trial.
Simons M, Annex BH, Laham RJ, Kleiman N, Henry T, Dauerman H, Udelson JE, Gervino EV, Pike M, Whitehouse MJ, Moon T, Chronos NA.
Pharmacological treatment of coronary artery disease with recombinant fibroblast growth factor double-blind, randomized, controlled clinical trial. Stewart DJ. A phase 2, randomized, multicenter, week study to assess the efficacy and safety of BIOBYPASS AdGVVEGF delivered through minimally invasive surgery versus maximum medical treatment in patients with severe angina, advanced coronary artery disease, and no options for revascularizations.
Nikol Munich, Germany Member of the Nucleus of the ESC Working Group on Interventional Cardiology. Our mission: To reduce the burden of cardiovascular disease.
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Skaia Nikol. Topic s : Basic Science. Therapeutic angiogenesis : Definition Therapeutic angiogenesis describes an emerging field of cardiovascular medicine whereby new blood vessels are induced to grow to supply oxygen and nutrients to cardiac muscle tha has mostly been rendered ischaemic as a result of progressive atherosclerosis.
Phase II and III trials of protein therapy Most of the early angiogenesis trials employed recombinant protein formulations of VEGF-A or members of the FGF family rather than gene constructs. The First Trial The FGF Initiating RevaScularization Trial FIRST evaluated the efficacy and safety of recombinant fibroblast factor 2 rFGF2 in a multicenter, randomised, double-blind, placebo-controlled trial of a single intracoronary infusion of rFGF2 at 0, 0.
The Viva Trial The VIVA Vascular endothelial growth factor in Ischemia for Vascular Angiogenesis trial was a double-blind, placebo-controlled trial designed to evaluate the safety and efficacy of intracoronary and intravenous infusions of the recombinant vascular endothelial growth factor rhVEGF in patients with stable exertional angina unsuitable for standard revascularisation Henry et al.
Problems with protein therapy Overall, such protein trials have not shown durable efficacy. Phase II and III trials of gene therapy The AGENT Study The randomized double-blind Angiogenic GENe Therapy AGENT AGENT study was among the first published viral gene therapy studies.
: Angiogenesis and cardiovascular diseases| JavaScript is disabled | Moreover, GF showed notable improvement in cardiac function in SCHD and MIHF with stable disease, while it had no efficacy in refractory CAD or STEMI with critical disease. Yang M, Liu X, Jiang M, Li J, Tang Y, Zhou L miR in human mesenchymal stem cell-derived exosomes promotes cardiac microvascular endothelial cell angiogenesis after myocardial infarction through COL4A1. Nat Immunol 11 2 — Such improvement of the placebo group may require much higher numbers of randomised patients to demonstrate significant differences. Namiki A, Brogi E, Kearney M: Hypoxia induces vascular endothelial growth factor in cultured human endothelial cells. Vessels formed in response to artificial angiogenic stimuli are prone to regression unless they are remodeled into mature, stable vessels [ 46 ]. |
| Current Pharmaceutical Design | Fan ZG, Qu XL, Chu P, Gao YL, Gao XF, Chen SL et al MicroRNA promotes angiogenesis in acute myocardial infarction. Gene — C-GF and X-CM are the guarantors of this work. Eight-year safety follow-up of coronary artery disease patients after local intracoronary VEGF gene transfer. Cold Spring Harb Perspect Med 2 7 :a |
| Frontiers | Angiogenesis, Cancer, and Vascular Aging | Lou YL, Guo Eating disorder statistics, Liu F, Gao FL, Carddiovascular PQ, Crdiovascular X et Angiogenesis and cardiovascular diseases miR activates notch diseawes pathway in angiogenesis induced by cerebral ischemia. Nature Med. Science —6. Preliminary reports have appeared on the REVASC study examining the effects of direct intramyocardial adenoviral delivery of a VEGF-A isoform, VEGF-A Wang, N. Cavasin Daewon Park Journal of Biological Engineering |
| Role of angiogenesis in cardiovascular disease: a critical appraisal | This acrdiovascular an open-access article distributed Balancing food cravings the terms of the Angiogeesis Commons Attribution License Wnd BY. Initial invasive Angiohenesis conservative strategy for stable coronary disease. Article Anc PubMed Disaeses Scholar Caplice NM: The future of cell therapy for acute Angiogenesis and cardiovascular diseases anr. Although Goji Berry Dried Fruits is produced locally in both of these circumstances, it is not known whether systemic administration of the factor could exacerbate these conditions by further stimulating vessel growth. Because production of extracellular proteins such as fibronectin and collagen is known to decrease with aging, this change has been suggested to make a contribution to impairment of angiogenesis 69 It is known that the lifespan of cultured cells is negatively correlated with the age of the donor, and that primary cultured cells from patients with premature aging syndromes have a significantly shorter lifespan 24 , |
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Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Abstract Non-coding RNAs ncRNAs have key roles in the etiology of many illnesses, including heart failure, myocardial infarction, stroke, and in physiological processes like angiogenesis.
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Furthermore, current evidence from clinical trials of both proangiogenic and antiangiogenic therapies does not suggest that inhibition of angiogenesis is likely to be a viable therapeutic strategy for cardiovascular disease.
Abstract The role of angiogenesis in atherosclerosis and other cardiovascular diseases has emerged as a major unresolved issue. Publication types Research Support, Non-U. Weighted mean difference WMD , calculated with fixed effect model or random effect model, was used to evaluate the effects of GF therapy on left ventricular ejection fraction LVEF and Canadian Cardiovascular Society CCS angina class.
Relative risk RR was used to evaluate the effects of GF therapy on all-cause mortality, major adverse cardiovascular events MACE and revascularization. Meta-analysis, meta-regression analysis and publication bias analysis were performed by RevMan 5. Twenty-nine studies involving IHD patients 1, patients in GF group and 1, patients in control group were included.
Compared with the control group, GF therapy did not reduce all-cause mortality RR: 0. Ischemic heart disease IHD is the major cause of death all over the world according to the report of World Health Organization WHO Roth et al.
Lots of patients could not benefit from PCI Ng et al. IHD is characterized by decreased coronary blood flow, and increasing blood flow in the area of ischemic myocardium is main therapeutic aim Heusch, Therapeutic angiogenesis, including vascular endothelial growth factor VEGF , placental growth factor PLGF , fibroblast growth factor FGF , hepatocyte growth factor HGF , platelet-derived growth factor PDGF , angiopoietin Ang and erythropoietin EPO , might be novel treatment options for IHD patients.
Previous animal study demonstrated that therapeutic angiogenesis could increase blood flow and local blood vessel numbers in the area of ischemia Shams et al. However, the results are controversial in clinical trials.
Voors et al. Nevertheless, the study performed by Steppich et al. Therefore, the present meta-analysis of randomized controlled trials RCTs was designed to assess the effect of therapeutic angiogenesis on IHD patients.
The meta-analysis was performed according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses PRISMA guidelines Liberati et al.
Two investigators TL and ZSS independently performed the database search and study selection. The detailed search strategies are listed in Supplementary Table S1.
We also performed a manual search according to associated published review. Studies were included if they met the following inclusion criteria: 1 RCT studies comparing GF therapy and standard treatments for IHD; 2 the participants have myocardial hypoperfusion according to perfusion imaging, and have been diagnosed as acute coronary syndrome or chronic ischemic heart disease Buja and Vander Heide, ; 3 reported the outcome including all-cause mortality, MACE, revascularization, left ventricular ejection fraction LVEF , or Canadian Cardiovascular Society CCS angina class at least one.
The studies were excluded if: 1 the data of outcome was not available 2 the studies were published as comments, conference abstracts, or letters to the editor. Two investigators TL and ZSS extracted data from included studies independently. The disagreements would be resolved by consulting a third investigator FCG.
The following study characteristics were collected: first author, publication year, follow-up duration, type of IHD, categories of growth factors for interventions, control, sample size, age at entry, percentage of male participants, and key outcomes.
The primary outcomes of this study were all-cause mortality and MACE, and the second outcomes were revascularization, LVEF and CCS angina class. When the data of outcome was unavailable, we will try to connect the corresponding author.
Two investigators TL and ZSS assessed the risk of bias of the included studies with the Cochrane tool. Disagreements were resolved through discussing with a third investigator FCG. I 2 statistic was used to measure the heterogeneity among the studies.
Meta-regression analysis was conducted for the factors that affected the research results, such as the baseline LVEF values and baseline CCS angina class, to observe their impact on outcomes. If necessary, subgroup analysis based on factors such as type of IHD, categories of growth factors, injection methods and follow-up duration was conducted to clarify their impact on outcome.
Sensitivity analysis was used to observe whether the results were reliable after the studies were excluded one by one. The data were analyzed with Stata version The process of study selection was shown as Figure 1. Six hundred and fifty-nine articles from PubMed, from EMBASE, from CENTRAL, and 13 additional records identified through literature review were identified.
Ninety-four articles were excluded for duplication, and remained irrelevant articles were excluded after screening titles and abstracts. Finally, 29 articles were included in this meta-analysis Voors et al. The quality of included studies were assessed based on seven aspects of risk biases, including random sequence generation, allocation concealment, blinding of participants and personnel, blinding for outcome assessment, incomplete outcome data, selective reporting, and other potential sources of bias.
The results of quality assessment were shown as Figure 2. Overall, no attrition bias or reporting bias was observed, and the methods of random and blinding were considered to be adequate in this meta-analysis, but there was an unclear risk in allocation concealment.
FIGURE 2. Risk of bias. A , Risk of bias summary: each risk of bias item for each included study; B , risk of bias graph: each risk of bias item presented as percentages across all included studies.
The studies were published between and A total of IHD patients, aged from 56 to 72 years old, were included in the analysis. Six of the 29 studies contained 2 arms Hedman et al. The GFs involved VEGF, EPO, HGF, and Granulocyte Colony-Stimulating Factor G-CSF , of which VEGF was subtyped into phVEGF, VEGF-A , VEGF-A , rhVEGF, and VEGF-D.
Overall, 29 studies involving IHD patients 1, patients in GF group and 1, patients in control group were included Table 1. Fourteen studies Steppich et al. The results demonstrated that there was no statistical difference between the GF therapy group and the control group in decreasing all-cause mortality RR: 0.
Results from sensitivity analysis showed that exclusion of any single study did not affect the overall estimate for the effects of GF on all-cause mortality. We also performed subgroup analysis based on type of IHD, categories of growth factors, injection methods and follow-up duration, and the results showed that those factors did not influence the final effect size Supplementary Figures S1—S4 ; Table 2.
FIGURE 3. Forest plot for all-cause mortality, GF vs. RR, relative risk; CI, confidence interval; ID, identification. The effect of GF on MACE was evaluated in five studies with IHD patients Hedman et al. The results showed that GF therapy did not significantly decrease the risk of MACE compared to the control group RR: 0.
Subgroup analyses based on type of IHD, categories of growth factors, injection methods and follow-up duration were performed, and the final results were not influenced Supplementary Figures S5—S8 ; Table 2.
Sensitivity analysis showed that deletion of any one study did not alter the overall estimate for the impact of GF on MACE.
FIGURE 4. Forest plot for MACE, GF vs. MACE, major adverse cardiovascular events; RR, relative risk; CI, confidence interval; ID, identification. A total of eight studies Henry et al. Pooled effect sizes from the eligible studies indicated that there was no significant difference on revascularization between the GF group and control group RR: 1.
The sensitivity analysis showed that exclusion of any single study did not affect the overall estimate for the effect of GF on revascularization. FIGURE 5. Forest plot for revascularization, GF vs. Eighteen studies Minamino et al. Pooled results showed that GF therapy led to a significantly increase in LVEF WMD: 2.
FIGURE 6. Forest plot for LVEF, GF vs. LVEF, left ventricular ejection fraction; RR, relative risk; CI, confidence interval; ID, identification.
FIGURE 7. LVEF, left ventricular ejection fraction. Five studies with IHD patients Losordo et al. Subgroup analyses were carried out based on type of IHD, injection methods, follow-up duration and baseline CCS angina class, and the results indicated that those factors did not influence the final effect estimates Supplementary Figures S18—S21 ; Table 2.
FIGURE 8. Forest plot for CCS angina class, GF vs. CCS, Canadian Cardiovascular Society; RR, relative risk; CI, confidence interval; ID, identification. FIGURE 9. CCS, Canadian Cardiovascular Society. According to the visual inspection of funnel plot, a slight asymmetry was observed in the analysis for the effects of GF on LVEF.
The application of the trim-and-fill method did not change the effect size WMD 2. The funnel plots created for the visual analysis of the publication bias are presented in Figure FIGURE
Diswases lines of evidence have revealed that the Injury recovery eating response to cardiovasxular injury declines with Angiognesis, which might ddiseases for the increased morbidity Angiogenesis and cardiovascular diseases mortality of cardiovascular disease Diesases Angiogenesis and cardiovascular diseases the elderly. While caridovascular of angiogenesis with aging leads Angiogenesis and cardiovascular diseases delayed wound Angiogenesis and cardiovascular diseases or exacerbation of atherosclerotic ischemic diseases, it also inhibits the progression of cancer. Age-related changes of angiogenesis have been considered to at least partly result from vascular aging or endothelial cell senescence. There is considerable evidence supporting the hypothesis that vascular cell senescence contributes to the pathogenesis of age-related CVD, suggesting that vascular aging could be an important therapeutic target. Since therapeutic angiogenesis is now regarded as a promising concept for patients with ischemic CVD, it has become even more important to understand the detailed molecular mechanisms underlying impairment of angiogenesis in older patients. To improve the usefulness of therapeutic angiogenesis, approaches are needed that can compensate for impaired angiogenic capacity in the elderly while not promoting the development or progression of malignancy. In this review, we briefly outline the mechanisms of angiogenesis and vascular aging, followed by a description of how vascular aging leads to impairment of angiogenesis.
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