The impact of vascular endothelial growth factor single nucleotide polymorphisms in the development and severity of endometriosis: A systematic review of the literature

Pergialiotis, Vasilios; Fanaki, Maria; Bellos, Ioannis; Stefanidis, Konstantinos; Loutradis, Dimitrios; Daskalakis, Georgios

doi:10.1016/j.jogoh.2020.101732

Cited by 3 publications

(5 citation statements)

References 38 publications

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“…The 26 animal DEGs that we have found to be homologous to the human hub genes for atherogenesis, atherosclerosis and atheroprotection are listed in the right-hand part of Table S4; the effects that changes in the expression levels of these hub genes have on human health are listed in the left-hand part. As can be seen from the bottom row of the table in Figure 1, the DEGs whose expression levels are higher in domestic than wild animals occur at significantly higher frequencies than they would have if they had been under neutral drift [32][33][34][35][36][37][38][39][40][41] (P ADJ < 0.05, binomial distribution with Bonferroni's correction). This is consistent with a case of destabilizing selection as a necessary attribute in animal domestication [222].…”

Section: Verification Of the Resultsmentioning

confidence: 99%

“…Finally, as the reader can see, with our resource-friendly in silico analysis of 5112 SNPs in the promoters of 16 hub genes for atherogenesis, atherosclerosis and atheroprotection, we have identified two candidate biomedical SNP markers, rs541151948:A and rs541151948:T, as being the most promising for a less resource-friendly cohort search for clinical SNP markers for personalized medicine, including their testing for the Hardy-Weinberg equilibrium [38].…”

Section: Verification Of the Resultsmentioning

confidence: 99%

“…Because personalized medicine [30] uses SNP markers of diseases for diagnosing these diseases and offering an adequate course of therapy, a comparison of representative cohorts of patients and healthy volunteers, including a test of Hardy-Weinberg equilibrium [38], should necessarily precede any clinical use of such markers. However, cohort studies are so demanding in terms of time, money and labor that it is just impractical to think of using them as a means to check whether or not each of more than 515,000 SNPs is a molecular marker of predisposition to something from among more than 55,000 diseases [39].…”

Section: Introductionmentioning

confidence: 99%

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Candidate SNP Markers Significantly Altering the Affinity of TATA-Binding Protein for the Promoters of Human Hub Genes for Atherogenesis, Atherosclerosis and Atheroprotection

Bogomolov

Filonov

Chadaeva

et al. 2023

IJMS

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Atherosclerosis is a systemic disease in which focal lesions in arteries promote the build-up of lipoproteins and cholesterol they are transporting. The development of atheroma (atherogenesis) narrows blood vessels, reduces the blood supply and leads to cardiovascular diseases. According to the World Health Organization (WHO), cardiovascular diseases are the leading cause of death, which has been especially boosted since the COVID-19 pandemic. There is a variety of contributors to atherosclerosis, including lifestyle factors and genetic predisposition. Antioxidant diets and recreational exercises act as atheroprotectors and can retard atherogenesis. The search for molecular markers of atherogenesis and atheroprotection for predictive, preventive and personalized medicine appears to be the most promising direction for the study of atherosclerosis. In this work, we have analyzed 1068 human genes associated with atherogenesis, atherosclerosis and atheroprotection. The hub genes regulating these processes have been found to be the most ancient. In silico analysis of all 5112 SNPs in their promoters has revealed 330 candidate SNP markers, which statistically significantly change the affinity of the TATA-binding protein (TBP) for these promoters. These molecular markers have made us confident that natural selection acts against underexpression of the hub genes for atherogenesis, atherosclerosis and atheroprotection. At the same time, upregulation of the one for atheroprotection promotes human health.

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Section: Verification Of the Resultsmentioning

confidence: 99%

Section: Verification Of the Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Candidate SNP Markers Significantly Altering the Affinity of TATA-Binding Protein for the Promoters of Human Hub Genes for Atherogenesis, Atherosclerosis and Atheroprotection

Bogomolov

Filonov

Chadaeva

et al. 2023

IJMS

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“…Em relação ao gene VEGF, os polimorfismos -2578 A/C e +936 C/T não foram associados à endometriose em pesquisa conduzida por Rashidi et al (2019), confirmando estudos prévios de revisão sistemática (PERGIALIOTIS et al, 2020) e meta-análise (MÉAR et al, 2020).…”

Section: Discussionunclassified

O Papel Dos Polimorfismos Genéticos Na Etiologia Da Endometriose

Colucci¹,

Cintra²,

Marqui³

2022

Arq. Ciênc. Saúde Unipar

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O objetivo desse estudo é apresentar uma atualização sobre o papel dos polimorfismos genéticos na etiologia da endometriose. Trata-se de uma pesquisa bibliográfica feita no PubMed utilizando os descritores “polymorphism and endometriosis”. Foram identificados 36 artigos e após aplicação dos critérios de inclusão foram selecionados 17 artigos para a amostra final. Os principais resultados foram: 1) cerca de 60% dos artigos foram publicados em 2019; 2) em 35,3% dos estudos o número de casos e controles investigados foi menor que 100; 3) a maioria dos trabalhos investigou de um a dois polimorfismos por gene; 4) a produção científica sobre endometriose é maior em países orientais; 5) houve heterogeneidade quanto aos periódicos onde os trabalhos foram publicados; 6) as principais técnicas para detecção de polimorfismos foi a PCR-RFLP e o PCR em tempo real, com frequências semelhantes. Em suma, os polimorfismos genéticos podem estar implicados na etiologia da endometriose.

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“…Vascular endothelial growth factor (VEGF) is an autocrine and paracrine growth factor that can improve vascular permeability, damage the tight junctions of vascular endothelial cells, induce endothelial cell proliferation, and promote extracellular fluid accumulation, vascular leakage, and neovascularization 5,6 . Matrix metalloproteinase-9 (MMP-9), one of the important protein hydrolases in the family of MMPs, disrupts basement membrane integrity and promotes neovascularization and vascular endothelial cell outgrowth, thus playing an important role in the ectopic implantation, adhesion, and growth of endometrial cells 7 .…”

Section: Introductionmentioning

confidence: 99%

Effects of SU5416 on angiogenesis and the ERK-VEGF/MMP-9 pathway in rat endometriosis.

Zhao,

Bao,

Chen

et al. 2023

Investigación Clínica

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SU5416 is a small molecule vascular endothelial growth factor (VEGF) receptor signal transduction inhibitor, which can block the VEGF re-ceptor autophosphorylation and inhibit receptor tyrosine kinase signal trans-duction, thereby reducing VEGF activity. However, there are few reports about the correlation of SU5416 to the occurrence and angiogenesis in endometrio-sis. In this study, we observed the effects of VEGF receptor inhibitor SU5416 on angiogenesis in endometriosis in rats. Thirty femalespecific-pathogen-free Sprague-Dawley rats were randomly divided into sham operation group (SOG), model group (MG), and SU5416 group (n=10 for each group). In the SOG, only the uterus was cut and sutured, and endometriosis models were established in the MG and SU5416 group by autologous transplantation. The SU5416 group was injected with 15 mg/kg SU5416 intraperitoneally, and the SOG and MG were intraperitoneally injected with an equal volume of normal saline for 6 weeks. The volume of ectopic lesions was lower in the SU5416 group at 42 d postoperatively thanin the MG (p<0.05). The proportion of CD31-positive cells in the endometrial tissue of the SU5416 group was lower than that of the MG (p<0.05); angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), laminin-5γ2 (LN-5γ2) and phosphorylation of ERK (P-ERK), VEGF, matrix metalloproteinase (MMP)-2, and MMP-9 protein expressions were lower in the SU5416 groupthan in the MG (p<0.05).VEGFreceptor inhibitor SU5416 can inhibit endometrio-sis angiogenesis and reduce inflammatory response in rats, and its mechanism of action may be related to the down-regulation of the ERK-VEGF/MMP-9 path-way expression.

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The impact of vascular endothelial growth factor single nucleotide polymorphisms in the development and severity of endometriosis: A systematic review of the literature

Cited by 3 publications

References 38 publications

Candidate SNP Markers Significantly Altering the Affinity of TATA-Binding Protein for the Promoters of Human Hub Genes for Atherogenesis, Atherosclerosis and Atheroprotection

Candidate SNP Markers Significantly Altering the Affinity of TATA-Binding Protein for the Promoters of Human Hub Genes for Atherogenesis, Atherosclerosis and Atheroprotection

O Papel Dos Polimorfismos Genéticos Na Etiologia Da Endometriose

Effects of SU5416 on angiogenesis and the ERK-VEGF/MMP-9 pathway in rat endometriosis.

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