Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular endothelial growth factor (VEGF), as an endothelial cell-specific mitogen, is crucial for new blood vessels formation. Atherosclerosis affecting the cardiovascular system causes ischemia and functio laesa in tissues supplied by the occluded vessels. When such a situation occurs in the lower extremities, it causes critical limb ischemia (CLI) often requiring leg amputation. Low oxygen tension leads to upregulation of hypoxia-regulated genes (i.e. VEGF), that should help to restore the impaired blood flow. In CLI these rescue mechanisms are, however, often inefficient. Moreover, there are many contradictory reports showing either induction, no changes or even down-regulation of VEGF in specimens taken from patients with CLI, as well as in samples collected from animals subjected to hindlimb ischemia. Additionally, taking into account numerous experimental and clinical data demonstrating rather insufficient therapeutic potential of VEGF, we called into question the role of this protein in limb ischemia and vessel regeneration. In this review we are also summarizing several aspects which can influence VEGF expression and its measurement in the ischemic tissues.
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PMID:Limb ischemia and vessel regeneration: Is there a role for VEGF? 2762 Aug 9

Psoriasis, a common disease affecting 2%-3% of the UK population, produces significant impairment of quality of life and is an immense burden on sufferers and their families. Psoriasis is associated with significant cardiovascular comorbidity and the metabolic syndrome. Angiogenesis, a relatively under-researched component of psoriasis, is a key factor in pathogenesis of psoriasis and also contributes to the development of atherosclerosis. Vascular endothelial growth factor (VEGF) is a well-established mediator of pathological angiogenesis which is upregulated in psoriasis. It is possible that, in patients with psoriasis, cutaneous angiogenesis may be both a marker for systemic vascular pathology and a novel therapeutic target. In this viewpoint study, the role of VEGF-mediated angiogenesis as a cause for cardiovascular events in patients with psoriasis is explored.
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PMID:Excessive angiogenesis associated with psoriasis as a cause for cardiovascular ischaemia. 2815 19

Peripheral vascular occlusive disease (PVOD) is a common manifestation of atherosclerosis, and it has a high rate of morbidity. Therapeutic angiogenesis would re-establish blood perfusion and rescue ischemic tissue. Vascular endothelial growth factor (VEGF) induces angiogenesis and can potentially be used to treat ischemic diseases, yet in clinical trials VEGF has not fulfilled its full potential with side effects. Whether amino acids promote angiogenesis and the molecular mechanisms are largely unknown. Here we showed that (1) Glycine significantly promoted angiogenesis both in vitro and in vivo and effectively protected mitochondrial function. (2) Activation of glycine transporter 1(GlyT1) induced by VEGF led to an increase in intracellular glycine. (3) Glycine directly bounded to voltage dependent anion channel 1 (VDAC1) on the mitochondrial outer membrane and inhibited its opening. These original results highlight glycine as a necessary mediator in VEGF signalling via the GlyT1-glycine-mTOR-VDAC1 axis pathway. Therefore, the findings in this study are of significance providing new mechanistic insights into angiogenesis and providing better understanding of glycine function in angiogenesis, which may provide valuable information for development of novel therapeutic targets for the treatment of angiogenic vascular disorders.
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PMID:Vascular endothelial growth factor signaling requires glycine to promote angiogenesis. 2911 38

Vascular endothelial growth factor (VEGF) is a promising molecule for cardiovascular diseases therapy. But lack of a targeted delivery system limits its translation into clinical application. This study aimed to develop stably overexpressing VEGF macrophages for targeted VEGF delivery to injured arteries and determine their potential for repairing of the damaged endothelium. Wire-induced carotid artery injury model was established in atherosclerosis-prone mice. It was observed that the VEGF-modified macrophages were recruited to the site of vascular injury and incorporated into new endothelium formation. VEGF-modified macrophages therapy accelerated reendothelialization and attenuated neointima formation. The VEGF protein level in tissues of injured arteries treated with VEGF-modified macrophages was increased. The upregulated C-C chemokine receptor type 5 (CCR5) and unaltered CCR2 protein levels were verified in VEGF-modified macrophages in vitro. Moreover, enhanced nitric oxide (NO) production in the culture medium of VEGF-modified macrophages was demonstrated. Our results indicated that VEGF-modified macrophages acted as vectors of VEGF targeting injured arteries, promoting the repairing directly by incorporating into new endothelium formation and indirectly by secreting sustainable VEGF and producing NO locally. This study represents a novel therapeutic application of targeted cell therapy with VEGF-modified macrophages for cardiovascular diseases.
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PMID:Vascular endothelial growth factor-modified macrophages accelerate reendothelialization and attenuate neointima formation after arterial injury in atherosclerosis-prone mice. 3064 9


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