Tse, H. Article CAS PubMed Herbal health remedies Scholar Angiogenesis and cardiovascular diseases W, Flamme Angiogenfsis Vasculogenesis. Diseasees longer and more stable gene expression, AAVs and genome-integrating lentiviruses may be considered with AAVs offering also serotype-specific tissue targeting. You can also search for this author in PubMed Google Scholar. Endocr Rev. This problem can also be circumvented by the use of gene therapy allowing for long-term over-expression of the target gene.

Angiogenesis and cardiovascular diseases -

Single intracoronary infusion of rFGF2 did not improve exercise tolerance, myocardial perfusion or angina symptoms at days significantly, due to continued improvement also seen in the placebo group. Adverse events were similar across all groups, except for hypotension, which occurred with higher frequency in the high-dose ?

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.

RhVEGF seemed to be safe and well tolerated. By day , only high-dose rhVEGF resulted in significant improvement in angina and favorable trends in exercise tolerance time and angina frequency. One unexpected and underestimated problem in those first angiogenic trials was the extent of improvement in the placebo group preventing those trials from turning out positive.

It is well known that good standard care including optimal medication and lifestyle changes - in particularly exercise - increases may induce the formation of collaterals via release of growth factors and progenitor cells.

Such improvement of the placebo group may require much higher numbers of randomised patients to demonstrate significant differences. Safety observations in some of the smaller trials and preclinical work have revealed dose-related proteinuria and transient hypotension, presumed to be due to activation of endothelial nitric oxide synthase eNOS and subsequent nitric oxide release.

Another more specific problem of protein therapy is the short half-life and residence time of most recombinant protein formulations, - probably too short considering that effective angiogenesis and arteriogenesis takes several months.

Targeted delivery to ischaemic zones of delayed release preparations of angiogenic peptides may yet prove efficacious. Clinical studies using this method of delivery are now in preclinical development. This problem can also be circumvented by the use of gene therapy allowing for long-term over-expression of the target gene.

Consequently, most remaining and ongoing angiogenic therapy trials for coronary heart disease have been or are conducted with genes, either using plasmid or an adenoviral vector.

The randomized double-blind Angiogenic GENe Therapy AGENT AGENT study was among the first published viral gene 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 delivered in a replication defective serotype 5 adenoviral vector Ad5-FGF4 to 79 patients with stable mild to moderate angina and no clinically significant heart failure.

Another objective was to select potentially safe and effective doses for subsequent study Grines et al. Transient, asymptomatic elevations in liver enzymes occurred in 2 patients in lower-dose groups that returned to the normal range within 4 weeks.

This was possibly related to the adenovirus 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 post-hoc analysis suggested that patients who received active 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.

Clinical trial design with appropriate endpoints is of critical importance. Claiming therapeutic effects without demonstration of the presence of the therapeutic protein should be avoided Figure 3.

It would be essential to design and validate surrogate markers for both transduction efficacy and biological activity of the gene product. Objective surrogate endpoint measurements, such as PET, MRI, ECG and ultrasound should be favoured instead of subjective or unspecific measures, such as exercise testing or quality of life questionnaires.

Also, the sensitivity of the methods employed should be re-evaluated as for example SPECT is not able to detect angiogenesis in the capillary level vessels. It may also be questioned whether endpoints like overall mortality, can reliably capture potentially significant treatment effects, such as number of hospital admissions or additional interventions in chronically ill aged individuals.

On the basis of the clinical trials in angiogenic gene therapy, there seems to be a clear disconnect between promising preclinical results and disappointments in RCTs. A re-evaluation is thus needed. While development of gene delivery vectors is still needed to improve gene transfer efficacy and gene expression in human tissues, the concept of therapeutic vascular growth in the treatment of CVD is evolving.

Affecting mainly the capillary level, angiogenic gene therapy might not be sufficient alone to promote revascularization in the scale of a human as compared to a laboratory mouse. Induction of lymphatic growth, to reduce revascularization- and angiogenesis-related oedema, might also be beneficial.

Additionally, as the recovery potential in animal models may differ significantly from that in the human patients, 44 the enhanced capillary level vascularity might not be enough to improve recovery of the severely affected and even necrotic human tissues.

The mitogenic and myogenic properties of e. HGF working besides angiogenesis might help to restore function and could explain some positive clinical results. Synergy with regenerative gene or cell therapies should also be considered.

Comorbidities and pharmacological treatments might have unpredictable effects on vascular growth. Gene transfer should yield high transduction efficiency in the target tissue without off-target side-effects.

Optimal duration and level of gene expression in angiogenic therapies has not yet been established. Subjective measures, such as exercise testing, may suffer from a significant placebo effect. Angiogenic gene therapy alone might not be sufficient to promote revascularization in large muscle areas.

Also, the growth of the whole vascular tree including lymphatics i. therapeutic vascular growth should be explored. Increasing capillary level vascularity might not be enough to enhance recovery in severely affected and even necrotic tissues. Supplementary material is available at European Heart Journal online.

This study was supported by Finnish Academy and Kuopio University Hospital, and by the National Institutes of Health grant 7-R01 HL Mozaffarian D , Benjamin EJ , Go AS , Arnett DK , Blaha MJ , Cushman M , de Ferranti S , Després JP , Fullerton HJ , Howard VJ , Huffman MD , Judd SE , Kissela BM , Lackland DT , Lichtman JH , Lisabeth LD , Liu S , Mackey RH , Matchar DB , McGuire DK , Mohler ER , Moy CS , Muntner P , Mussolino ME , Nasir K , Neumar RW , Nichol G , Palaniappan L , Pandey DK , Reeves MJ , Rodriguez CJ , Sorlie PD , Stein J , Towfighi A , Turan TN , Virani SS , Willey JZ , Woo D , Yeh RW , Turner MB.

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Cell Cycle 7 14 — J Orthop Res 25 7 — Wirrig EE, Yutzey KE Conserved transcriptional regulatory mechanisms in aortic valve development and disease.

Arterioscler Thromb Vasc Biol 34 4 — Cheng GZ, Zhang W, Wang L-H Regulation of cancer cell survival, migration, and invasion by Twist: AKT2 comes to interplay. Can Res 68 4 — Cancer Discov 2 3 — Ann Transl Med 8 14 Liu H, Li J, Koirala P, Ding X, Chen B, Wang Y et al Long non-coding RNAs as prognostic markers in human breast cancer.

Oncotarget 7 15 Michalik KM, You X, Manavski Y, Doddaballapur A, Zörnig M, Braun T et al Long noncoding RNA MALAT1 regulates endothelial cell function and vessel growth.

Circ Res 9 — Hutter R, Speidl WS, Valdiviezo C, Sauter B, Corti R, Fuster V et al Macrophages transmit potent proangiogenic effects of oxLDL in vitro and in vivo involving HIF-1α activation: a novel aspect of angiogenesis in atherosclerosis. J Cardiovasc Transl Res 6 4 — Perrotta I, Moraca FM, Sciangula A, Aquila S, Mazzulla S HIF-1α and VEGF: immunohistochemical profile and possible function in human aortic valve stenosis.

Ultrastruct Pathol 39 3 — Deng W, Feng X, Li X, Wang D, Sun L Hypoxia-inducible factor 1 in autoimmune diseases. Cell Immunol — Bao MH, Li GY, Huang XS, Tang L, Dong LP, Li JM Long Noncoding RNA LINC acting as a miRp sponge to facilitate low concentration oxidized low-density lipoprotein-induced angiogenesis.

Mol Pharmacol 93 4 — Chen ZL, Chen YX, Zhou J, Li Y, Gong CY, Wang XB LncRNA HULC alleviates HUVEC inflammation and improves angiogenesis after myocardial infarction through down-regulating miRb. Eur Rev Med Pharmacol Sci 24 11 — PubMed Google Scholar.

Li X, Sun Y, Huang S, Chen Y, Chen X, Li M et al Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway.

EBioMedicine — Neuropsychiatr Dis Treat — Brain Res Bull — Cell Mol Neurobiol 41 6 — Aging Albany NY 12 2 — Am J Transl Res 11 10 — Long FQ, Su QJ, Zhou JX, Wang DS, Li PX, Zeng CS et al LncRNA SNHG12 ameliorates brain microvascular endothelial cell injury by targeting miRa.

Neural Regen Res 13 11 — Wang Z, Wang R, Wang K, Liu X Upregulated long noncoding RNA Snhg1 promotes the angiogenesis of brain microvascular endothelial cells after oxygen-glucose deprivation treatment by targeting miRa. Can J Physiol Pharmacol 96 9 — Li L, Wang M, Mei Z, Cao W, Yang Y, Wang Y et al lncRNAs HIF1A-AS2 facilitates the up-regulation of HIF-1α by sponging to miRp, whereby promoting angiogenesis in HUVECs in hypoxia.

Biomed Pharmacother — Cell Cycle — Tzavlaki K, Moustakas A TGF-β Signaling. Biomolecules 10 3 Benn A, Hiepen C, Osterland M, Schütte C, Zwijsen A, Knaus P Role of bone morphogenetic proteins in sprouting angiogenesis: differential BMP receptor-dependent signaling pathways balance stalk vs.

tip cell competence. FASEB J 31 11 — Neuro Oncol 17 2 — J Cell Biol 6 — Genes Dev 29 12 — Zhao B, Wei X, Li W, Udan RS, Yang Q, Kim J et al Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control.

Genes Dev 21 21 — Park GS, Oh H, Kim M, Kim T, Johnson RL, Irvine KD et al An evolutionarily conserved negative feedback mechanism in the Hippo pathway reflects functional difference between LATS1 and LATS2. Oncotarget 7 17 — Zhao B, Lei QY, Guan KL The Hippo-YAP pathway: new connections between regulation of organ size and cancer.

Curr Opin Cell Biol 20 6 — Murakami H, Mizuno T, Taniguchi T, Fujii M, Ishiguro F, Fukui T et al LATS2 is a tumor suppressor gene of malignant mesothelioma. Cancer Res 71 3 — Cell Rep 5 6 — Yao F, Liu H, Li Z, Zhong C, Fang W Down-regulation of LATS2 in non-small cell lung cancer promoted the growth and motility of cancer cells.

Tumour Biol 36 3 — Ji T, Liu D, Shao W, Yang W, Wu H, Bian X Decreased expression of LATS1 is correlated with the progression and prognosis of glioma.

J Exp Clin Cancer Res 31 1 Zhang H, Sun J, Ju W, Li B, Lou Y, Zhang G et al Apatinib suppresses breast cancer cells proliferation and invasion via angiomotin inhibition. Am J Transl Res 11 7 — Cell 6 — Gao WQ, Hu XM, Zhang Q, Yang L, Lv XZ, Chen S et al Downregulation of circFASTKD1 ameliorates myocardial infarction by promoting angiogenesis.

Aging Albany NY 13 3 — Fu J, Bai P, Chen Y, Yu T, Li F Inhibition of miR improves both vascular remodeling and angiogenesis in pulmonary hypertension. J Vasc Res 56 2 — Gerald D, Adini I, Shechter S, Perruzzi C, Varnau J, Hopkins B et al RhoB controls coordination of adult angiogenesis and lymphangiogenesis following injury by regulating VEZF1-mediated transcription.

Nat Commun Article ADS PubMed Google Scholar. Jin F, Xing J Circulating pro-angiogenic and anti-angiogenic microRNA expressions in patients with acute ischemic stroke and their association with disease severity. Neurol Sci 38 11 — Jin F, Xing J Circulating miR and miRa levels correlate with lower disease risk, disease severity, and reduced inflammatory cytokine levels in acute ischemic stroke patients.

Neurol Sci 39 10 — Metab Brain Dis 36 8 — Cao X, He W, Pang Y, Cao Y, Qin A Redox-dependent and independent effects of thioredoxin interacting protein. Biol Chem 11 — Chistiakov DA, Orekhov AN, Bobryshev YV Effects of shear stress on endothelial cells: go with the flow.

Acta Physiol 2 — Mohamed IN, Ishrat T, Fagan SC, El-Remessy AB Role of inflammasome activation in the pathophysiology of vascular diseases of the neurovascular unit. Antioxid Redox Signal 22 13 — Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J Thioredoxin-interacting protein links oxidative stress to inflammasome activation.

Nat Immunol 11 2 — Masola V, Carraro A, Granata S, Signorini L, Bellin G, Violi P et al In vitro effects of interleukin IL -1 beta inhibition on the epithelial-to-mesenchymal transition EMT of renal tubular and hepatic stellate cells.

J Transl Med 17 1 Ushio-Fukai M, Nakamura Y Reactive oxygen species and angiogenesis: NADPH oxidase as target for cancer therapy. Cancer Lett 1 — Oxid Med Cell Longev Li J, Yue Z, Xiong W, Sun P, You K, Wang J TXNIP overexpression suppresses proliferation and induces apoptosis in SMMC cells through ROS generation and MAPK pathway activation.

Oncol Rep 37 6 — Byon CH, Han T, Wu J, Hui ST Txnip ablation reduces vascular smooth muscle cell inflammation and ameliorates atherosclerosis in apolipoprotein E knockout mice. Atherosclerosis 2 — Wang J, Wang X-J, Zhang Y, Shi W-J, Lei Z-D, Jiao X-Y TXNIP knockout improves cardiac function after myocardial infarction by promoting angiogenesis and reducing cardiomyocyte apoptosis.

Cardiovasc Diagnosis Therapy 12 3 Cent Eur J Immunol 47 1 — Su X, Wang J, Chen W, Li Z, Fu X, Yang A Overexpression of TRIM14 promotes tongue squamous cell carcinoma aggressiveness by activating the NF-κB signaling pathway. Oncotarget 7 9 Huang X, Li Y, Li X, Fan D, Xin HB, Fu M TRIM14 promotes endothelial activation via activating NF-κB signaling pathway.

J Mol Cell Biol 12 3 — BMC Cardiovasc Disord 21 1 Eur Rev Med Pharmacol Sci 24 1 — Wang T, Ren Y, Liu R, Ma J, Shi Y, Zhang L et al miRp suppresses the proliferation, migration, and invasion of oral squamous cell carcinoma by targeting TRIM Aging Albany NY 13 2 — Nenasheva VV, Kovaleva GV, Khaidarova NV, Novosadova EV, Manuilova ES, Antonov SA et al Trim14 overexpression causes the same transcriptional changes in mouse embryonic stem cells and human HEK cells.

In Vitro Cell Dev Biol Anim 50 2 — Si X, Zheng H, Wei G, Li M, Li W, Wang H et al circRNA Hipk3 induces cardiac regeneration after myocardial infarction in mice by binding to Notch1 and miRa.

Mol Therapy Nucleic Acsids — Zhang M, Wang Z, Cheng Q, Wang Z, Lv X, Wang Z et al Circular RNA circRNA CDYL Induces myocardial regeneration by ceRNA after myocardial infarction. Med Sci Monit e NeuroReport 33 4 — Bai X, Liu X, Wu H, Feng J, Chen H, Zhou D CircFUNDC1 knockdown alleviates oxygen-glucose deprivation-induced human brain microvascular endothelial cell injuries by inhibiting PTEN via miR Neurosci Lett Genes Genomics 44 9 — J Surg Res — Cardiovasc Drugs Ther 4 9 — J Thromb Thrombolysis 53 2 — Chang W, Wang J Exosomes and their noncoding RNA cargo are emerging as new modulators for diabetes mellitus.

Cells 8 8 Yoon YJ, Kim OY, Gho YS Extracellular vesicles as emerging intercellular communicasomes. BMB Rep 47 10 — Mathieu M, Martin-Jaular L, Lavieu G, Théry C Specificities of secretion and uptake of exosomes and other extracellular vesicles for cell-to-cell communication.

Nat Cell Biol 21 1 :9— Raposo G, Stoorvogel W Extracellular vesicles: exosomes, microvesicles, and friends. J Cell Biol 4 — Nat Rev Mol Cell Biol 19 4 — Jafari A, Babajani A, Abdollahpour-Alitappeh M, Ahmadi N, Rezaei-Tavirani M Exosomes and cancer: from molecular mechanisms to clinical applications.

Med Oncol 38 4 Acta Biomater — Xiong F, Mao R, Zhao R, Zhang L, Tan K, Liu C et al Plasma exosomal S1PR5 and CARNS1 as potential non-invasive screening biomarkers of coronary heart disease. Front Cardiovasc Med Sci Rep 10 1 Zaborowski MP, Balaj L, Breakefield XO, Lai CP Extracellular vesicles: composition, biological relevance, and methods of study.

Bioscience 65 8 — Dai J, Su Y, Zhong S, Cong L, Liu B, Yang J et al Exosomes: key players in cancer and potential therapeutic strategy.

Signal Transduct Target Ther 5 1 Urbanelli L, Magini A, Buratta S, Brozzi A, Sagini K, Polchi A et al Signaling pathways in exosomes biogenesis, secretion and fate.

Genes 4 2 — Kalluri R, LeBleu VS The biology, function, and biomedical applications of exosomes. Science Saad MG, Beyenal H, Dong WJ Exosomes as Powerful engines in cancer: isolation, characterization and detection techniques. Biosensors 11 12 Zhang Y, Liu Y, Liu H, Tang WH Exosomes: biogenesis, biologic function and clinical potential.

Cell Biosci Record M, Carayon K, Poirot M, Silvente-Poirot S Exosomes as new vesicular lipid transporters involved in cell-cell communication and various pathophysiologies. Biochem Biophys Acta 1 —

Trials cardiovascluar 2Article number: Angiogenesis and cardiovascular diseases this article. Metrics details. The identification of angiogenic growth factors, such Angiogenesis and cardiovascular diseases cadiovascular endothelial growth factor and cardiovacsular growth factor, has fueled interest in using Poppy seed salad dressing factors to induce therapeutic angiogenesis. The results of numerous animal studies and clinical trials have offered promise for new treatment strategies for various ischemic diseases. Increased understanding of the cellular and molecular biology of vessel growth has, however, prompted investigators and clinicians alike to reconsider the complexity of therapeutic angiogenesis. The realization that formation of a stable vessel is a complex, multistep process may provide useful insights into the design of the next generation of angiogenesis therapy.

Angiogenesis and cardiovascular diseases -

Current Angiogenesis Discontinued Editor-in-Chief: Guo-Chang Fan Dept. Editorial Editorial Thematic Issue: Angiogenesis in the Development of Cardiovascular Diseases Author s : College of Medicine Alfaisal University Box , Riyadh Kingdom of Saudi Arabia.

Purchase PDF. Mark Item. Current Angiogenesis Discontinued. Title: Editorial Thematic Issue: Angiogenesis in the Development of Cardiovascular Diseases Volume: 3 Issue: 1 Author s : Pallab Paul Ganguly Affiliation: Abstract: The role of angiogenesis in the development of cardiovascular diseases has been a great controversy in the recent past.

Close Print this page. Export Options ×. Export File: RIS for EndNote, Reference Manager, ProCite. Content: Citation Only. Citation and Abstract. About this article ×. Cite this article as: Ganguly Paul Pallab, Editorial Thematic Issue: Angiogenesis in the Development of Cardiovascular Diseases , Current Angiogenesis Discontinued ; 3 1.

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Cell J 18 1 :7— Nallamshetty S, Chan SY, Loscalzo J Hypoxia: a master regulator of microRNA biogenesis and activity. Free Radic Biol Med — Zhao X, Wei X, Wang X, Qi G Long non-coding RNA NORAD regulates angiogenesis of human umbilical vein endothelial cells via miRp under hypoxic conditions.

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Apoplexy Nervous Dis 33 2 — Fang Y, Davies PF Site-specific microRNAa regulation of Krüppel-like factors 4 and 2 in atherosusceptible endothelium. Arterioscler Thromb Vasc Biol 32 4 — Sangwung P, Zhou G, Nayak L, Chan ER, Kumar S, Kang D-W et al KLF2 and KLF4 control endothelial identity and vascular integrity.

JCI Insight 2 4 Zhang X, Wang L, Han Z, Dong J, Pang D, Fu Y et al KLF4 alleviates cerebral vascular injury by ameliorating vascular endothelial inflammation and regulating tight junction protein expression following ischemic stroke.

J Neuroinflammation 17 1 :1— Yang H, Xi X, Zhao B, Su Z, Wang Z KLF4 protects brain microvascular endothelial cells from ischemic stroke induced apoptosis by transcriptionally activating MALAT1. Biochem Biophys Res Commun 3 — Wang C, Dong J, Sun J, Huang S, Wu F, Zhang X et al Silencing of lncRNA XIST impairs angiogenesis and exacerbates cerebral vascular injury after ischemic stroke.

Mol Ther Nucleic Acids — Nurnberg ST, Guerraty MA, Wirka RC, Rao HS, Pjanic M, Norton S et al Genomic profiling of human vascular cells identifies TWIST1 as a causal gene for common vascular diseases. PLoS Genet 16 1 :e Mammoto A, Hendee K, Muyleart M, Mammoto T Endothelial Twist1-PDGFB signaling mediates hypoxia-induced proliferation and migration of αSMA-positive cells.

Sci Rep 10 1 :1— Mahmoud MM, Kim HR, Xing R, Hsiao S, Mammoto A, Chen J et al TWIST1 integrates endothelial responses to flow in vascular dysfunction and atherosclerosis. Circ Res 3 — Li J, Liu C-H, Sun Y, Gong Y, Fu Z, Evans LP et al Endothelial TWIST1 promotes pathological ocular angiogenesis.

Invest Ophthalmol Vis Sci 55 12 — Mammoto T, Jiang A, Jiang E, Mammoto A Role of Twist1 phosphorylation in angiogenesis and pulmonary fibrosis. Am J Respir Cell Mol Biol 55 5 — Mammoto T, Jiang E, Jiang A, Lu Y, Juan AM, Chen J et al Twist1 controls lung vascular permeability and endotoxin-induced pulmonary edema by altering Tie2 expression.

PLoS ONE 8 9 :e Kaushik K, Das A TWIST1-Reprogrammed endothelial cell transplantation potentiates neovascularization-mediated diabetic wound tissue regeneration.

Diabetes 69 6 — Chen H-F, Huang C-H, Liu C-J, Hung J-J, Hsu C-C, Teng S-C et al Twist1 induces endothelial differentiation of tumour cells through the Jagged1-KLF4 axis. ADS Google Scholar.

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Am J Respir Cell Mol Biol 58 2 — Yang M-H, Wu K-J TWIST activation by hypoxia inducible factor-1 HIF-1 : implications in metastasis and development. Cell Cycle 7 14 — J Orthop Res 25 7 — Wirrig EE, Yutzey KE Conserved transcriptional regulatory mechanisms in aortic valve development and disease.

Arterioscler Thromb Vasc Biol 34 4 — Cheng GZ, Zhang W, Wang L-H Regulation of cancer cell survival, migration, and invasion by Twist: AKT2 comes to interplay. Can Res 68 4 — Cancer Discov 2 3 — Ann Transl Med 8 14 Liu H, Li J, Koirala P, Ding X, Chen B, Wang Y et al Long non-coding RNAs as prognostic markers in human breast cancer.

Oncotarget 7 15 Michalik KM, You X, Manavski Y, Doddaballapur A, Zörnig M, Braun T et al Long noncoding RNA MALAT1 regulates endothelial cell function and vessel growth.

Circ Res 9 — Hutter R, Speidl WS, Valdiviezo C, Sauter B, Corti R, Fuster V et al Macrophages transmit potent proangiogenic effects of oxLDL in vitro and in vivo involving HIF-1α activation: a novel aspect of angiogenesis in atherosclerosis.

J Cardiovasc Transl Res 6 4 — Perrotta I, Moraca FM, Sciangula A, Aquila S, Mazzulla S HIF-1α and VEGF: immunohistochemical profile and possible function in human aortic valve stenosis.

Ultrastruct Pathol 39 3 — Deng W, Feng X, Li X, Wang D, Sun L Hypoxia-inducible factor 1 in autoimmune diseases. Cell Immunol — Bao MH, Li GY, Huang XS, Tang L, Dong LP, Li JM Long Noncoding RNA LINC acting as a miRp sponge to facilitate low concentration oxidized low-density lipoprotein-induced angiogenesis.

Mol Pharmacol 93 4 — Chen ZL, Chen YX, Zhou J, Li Y, Gong CY, Wang XB LncRNA HULC alleviates HUVEC inflammation and improves angiogenesis after myocardial infarction through down-regulating miRb.

Eur Rev Med Pharmacol Sci 24 11 — PubMed Google Scholar. Li X, Sun Y, Huang S, Chen Y, Chen X, Li M et al Inhibition of AZIN2-sv induces neovascularization and improves prognosis after myocardial infarction by blocking ubiquitin-dependent talin1 degradation and activating the Akt pathway.

EBioMedicine — Neuropsychiatr Dis Treat — Brain Res Bull — Cell Mol Neurobiol 41 6 — Aging Albany NY 12 2 — Am J Transl Res 11 10 — Long FQ, Su QJ, Zhou JX, Wang DS, Li PX, Zeng CS et al LncRNA SNHG12 ameliorates brain microvascular endothelial cell injury by targeting miRa.

Neural Regen Res 13 11 — Wang Z, Wang R, Wang K, Liu X Upregulated long noncoding RNA Snhg1 promotes the angiogenesis of brain microvascular endothelial cells after oxygen-glucose deprivation treatment by targeting miRa.

Can J Physiol Pharmacol 96 9 — Li L, Wang M, Mei Z, Cao W, Yang Y, Wang Y et al lncRNAs HIF1A-AS2 facilitates the up-regulation of HIF-1α by sponging to miRp, whereby promoting angiogenesis in HUVECs in hypoxia.

Biomed Pharmacother — Cell Cycle — Tzavlaki K, Moustakas A TGF-β Signaling. Biomolecules 10 3 Benn A, Hiepen C, Osterland M, Schütte C, Zwijsen A, Knaus P Role of bone morphogenetic proteins in sprouting angiogenesis: differential BMP receptor-dependent signaling pathways balance stalk vs.

tip cell competence. FASEB J 31 11 — Neuro Oncol 17 2 — J Cell Biol 6 — Genes Dev 29 12 — Zhao B, Wei X, Li W, Udan RS, Yang Q, Kim J et al Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control.

Genes Dev 21 21 — Park GS, Oh H, Kim M, Kim T, Johnson RL, Irvine KD et al An evolutionarily conserved negative feedback mechanism in the Hippo pathway reflects functional difference between LATS1 and LATS2.

Oncotarget 7 17 — Zhao B, Lei QY, Guan KL The Hippo-YAP pathway: new connections between regulation of organ size and cancer. Curr Opin Cell Biol 20 6 — Murakami H, Mizuno T, Taniguchi T, Fujii M, Ishiguro F, Fukui T et al LATS2 is a tumor suppressor gene of malignant mesothelioma. Cancer Res 71 3 — Cell Rep 5 6 — Yao F, Liu H, Li Z, Zhong C, Fang W Down-regulation of LATS2 in non-small cell lung cancer promoted the growth and motility of cancer cells.

Tumour Biol 36 3 — Ji T, Liu D, Shao W, Yang W, Wu H, Bian X Decreased expression of LATS1 is correlated with the progression and prognosis of glioma. J Exp Clin Cancer Res 31 1 Zhang H, Sun J, Ju W, Li B, Lou Y, Zhang G et al Apatinib suppresses breast cancer cells proliferation and invasion via angiomotin inhibition.

Am J Transl Res 11 7 — Cell 6 — Gao WQ, Hu XM, Zhang Q, Yang L, Lv XZ, Chen S et al Downregulation of circFASTKD1 ameliorates myocardial infarction by promoting angiogenesis. Aging Albany NY 13 3 — Fu J, Bai P, Chen Y, Yu T, Li F Inhibition of miR improves both vascular remodeling and angiogenesis in pulmonary hypertension.

J Vasc Res 56 2 — Gerald D, Adini I, Shechter S, Perruzzi C, Varnau J, Hopkins B et al RhoB controls coordination of adult angiogenesis and lymphangiogenesis following injury by regulating VEZF1-mediated transcription.

Nat Commun Article ADS PubMed Google Scholar. Jin F, Xing J Circulating pro-angiogenic and anti-angiogenic microRNA expressions in patients with acute ischemic stroke and their association with disease severity. Neurol Sci 38 11 — Jin F, Xing J Circulating miR and miRa levels correlate with lower disease risk, disease severity, and reduced inflammatory cytokine levels in acute ischemic stroke patients.

Neurol Sci 39 10 — Metab Brain Dis 36 8 — Cao X, He W, Pang Y, Cao Y, Qin A Redox-dependent and independent effects of thioredoxin interacting protein.

Biol Chem 11 — Chistiakov DA, Orekhov AN, Bobryshev YV Effects of shear stress on endothelial cells: go with the flow. Acta Physiol 2 — Mohamed IN, Ishrat T, Fagan SC, El-Remessy AB Role of inflammasome activation in the pathophysiology of vascular diseases of the neurovascular unit.

Antioxid Redox Signal 22 13 — Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J Thioredoxin-interacting protein links oxidative stress to inflammasome activation.

Nat Immunol 11 2 — Masola V, Carraro A, Granata S, Signorini L, Bellin G, Violi P et al In vitro effects of interleukin IL -1 beta inhibition on the epithelial-to-mesenchymal transition EMT of renal tubular and hepatic stellate cells. J Transl Med 17 1 Ushio-Fukai M, Nakamura Y Reactive oxygen species and angiogenesis: NADPH oxidase as target for cancer therapy.

Cancer Lett 1 — Oxid Med Cell Longev Li J, Yue Z, Xiong W, Sun P, You K, Wang J TXNIP overexpression suppresses proliferation and induces apoptosis in SMMC cells through ROS generation and MAPK pathway activation.

Oncol Rep 37 6 — Byon CH, Han T, Wu J, Hui ST Txnip ablation reduces vascular smooth muscle cell inflammation and ameliorates atherosclerosis in apolipoprotein E knockout mice. Atherosclerosis 2 — Wang J, Wang X-J, Zhang Y, Shi W-J, Lei Z-D, Jiao X-Y TXNIP knockout improves cardiac function after myocardial infarction by promoting angiogenesis and reducing cardiomyocyte apoptosis.

Cardiovasc Diagnosis Therapy 12 3 Cent Eur J Immunol 47 1 — Su X, Wang J, Chen W, Li Z, Fu X, Yang A Overexpression of TRIM14 promotes tongue squamous cell carcinoma aggressiveness by activating the NF-κB signaling pathway.

Oncotarget 7 9 Huang X, Li Y, Li X, Fan D, Xin HB, Fu M TRIM14 promotes endothelial activation via activating NF-κB signaling pathway. J Mol Cell Biol 12 3 — BMC Cardiovasc Disord 21 1 Eur Rev Med Pharmacol Sci 24 1 — Wang T, Ren Y, Liu R, Ma J, Shi Y, Zhang L et al miRp suppresses the proliferation, migration, and invasion of oral squamous cell carcinoma by targeting TRIM Aging Albany NY 13 2 — Nenasheva VV, Kovaleva GV, Khaidarova NV, Novosadova EV, Manuilova ES, Antonov SA et al Trim14 overexpression causes the same transcriptional changes in mouse embryonic stem cells and human HEK cells.

In Vitro Cell Dev Biol Anim 50 2 — Si X, Zheng H, Wei G, Li M, Li W, Wang H et al circRNA Hipk3 induces cardiac regeneration after myocardial infarction in mice by binding to Notch1 and miRa.

Mol Therapy Nucleic Acsids — Zhang M, Wang Z, Cheng Q, Wang Z, Lv X, Wang Z et al Circular RNA circRNA CDYL Induces myocardial regeneration by ceRNA after myocardial infarction.

Med Sci Monit e NeuroReport 33 4 — Bai X, Liu X, Wu H, Feng J, Chen H, Zhou D CircFUNDC1 knockdown alleviates oxygen-glucose deprivation-induced human brain microvascular endothelial cell injuries by inhibiting PTEN via miR Neurosci Lett Genes Genomics 44 9 — J Surg Res — Cardiovasc Drugs Ther 4 9 — J Thromb Thrombolysis 53 2 — Chang W, Wang J Exosomes and their noncoding RNA cargo are emerging as new modulators for diabetes mellitus.

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Angogenesis Ylä-Herttuala, Diseasees Bridges, Michael G. Katz, Petra Korpisalo, Angiogenesis and cardiovascular diseases gene therapy in cardiovascular diseases: dream cardiocascular vision? Chronic cardiovascular diseases are acrdiovascular health problems. Angiogenesis and cardiovascular diseases therapy and therapeutic vascular growth may provide a new treatment option for these patients. Several growth factors, like vascular endothelial growth factors, fibroblast growth factors and hepatocyte growth factor have been tested in clinical trials. However, apart from demonstration of increased vascularity, very few results with clinical significance have been obtained.