Association of TGF-β1 gene polymorphisms in exon1 and blood levels with essential hypertension

He, Fang; Zhao, Dan; Deng, Feng-mei; Zhong, Hua; Shi, Xiaopeng; Yang, Jianfeng; Guo, Shuxia; Cheng, Jason Chia‐Hsien; Huang, Gang; Tang, Bin; Wang, Zhenhuan; Chen, Xiongying; Wang, Gang; Zhang, Wanjiang; Zhang, Chunjun; Wang, Xuewen; Hu, Qinghua

doi:10.3109/08037051003768254

Cited by 11 publications

(10 citation statements)

References 28 publications

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“…Furthermore, TGF-β affects endothelial cells in numerous ways, notably altering the nitric oxide pathway to impair flow-induced relaxation (Buday et al 2010). Polymorphisms in TGF-β are associated with essential hypertension in Chinese ethnic subgroups (He et al 2010). Elevated TGF-β levels associated with TGF-β single nucleotide polymorphisms might also be a contributing factor to renal disease, a major cause of hypertension (August et al 2009).…”

Section: Component Factors In the Etiology Of Atherosclerosismentioning

confidence: 99%

Transforming growth factor-β and atherosclerosis: interwoven atherogenic and atheroprotective aspects

2011

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Age-related progression of cardiovascular disease is by far the largest health problem in the US and involves vascular damage, progressive vascular fibrosis and the accumulation of lipid-rich atherosclerotic lesions. Advanced lesions can restrict flow to key organs and can trigger occlusive thrombosis resulting in a stroke or myocardial infarction. Transforming growth factor-beta (TGF-β) is a major orchestrator of the fibroproliferative response to tissue damage. In the early stages of repair, TGF-β is released from platelets and activated from matrix reservoirs; it then stimulates the chemotaxis of repair cells, modulates immunity and inflammation and induces matrix production. At later stages, it negatively regulates fibrosis through its strong antiproliferative and apoptotic effects on fibrotic cells. In advanced lesions, TGF-β might be important in arterial calcification, commonly referred to as “hardening of the arteries”. Because TGF-β can signal through multiple pathways, namely the SMADs, a MAPK pathway and the Rho/ROCK pathways, selective defects in TGF-β signaling can disrupt otherwise coordinated pathways of tissue regeneration. TGF-β is known to control cell proliferation, cell migration, matrix synthesis, wound contraction, calcification and the immune response, all being major components of the atherosclerotic process. However, many of the effects of TGF-β are essential to normal tissue repair and thus, TGF-β is often thought to be “atheroprotective”. The present review attempts to parse systematically the known effects of TGF-β on both the major risk factors for atherosclerosis and to isolate the role of TGF-β in the many component pathways involved in atherogenesis.

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Section: Component Factors In the Etiology Of Atherosclerosismentioning

confidence: 99%

Transforming growth factor-β and atherosclerosis: interwoven atherogenic and atheroprotective aspects

2011

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“…TGF 915 G>C polymorphism is related to left bentricular hypertrophy in hypertensives [58]. 896 T>C is associated with essential hypertension in Chinese [59]. Those observations indicate that polymorphisms in the TGF-β 1 gene may be involved in the pathological development of hypertension.…”

Section: Discussionmentioning

confidence: 81%

Polymorphisms and Plasma Level of Transforming Growth Factor-Beta 1 and Risk for Preeclampsia: A Systematic Review

Shen

Tan

2014

PLoS ONE

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BackgroundTransforming growth factor-beta 1 (TGF-β1) is thought to be involved in the pathogenesis of preeclampsia (PE), but the results are inconsistent among studies. This article aims to compile an overview of the studies about the associations of TGF-β 1 polymorphism and plasma level with PE risk and to provide recommendations for future research.Methods and ResultsThe databases PubMed, Embase and Web of Science were searched up to December 2013. Five studies investigating the associations of four polymorphisms with the risks of PE were involved. A meta-analysis was conducted for the 869T>C polymorphism and PE risk. The results show that genotype TT of 869T>C polymorphism is a protective factor of PE (pooled odds ratio = 0.73, 95% CI: 0.56, 0.95). Eight case-control studies reported the plasma level of TGF-β 1. The substantial heterogeneity among studies may be attributed to the differences in the blood sample processing and the TGF-β 1 analysis kits. The results suggest that plasma TGF-β 1 level in the second trimester was significantly lower in the PE group than in the normal pregnancy group, but was significantly higher in the PE group during the third trimester.ConclusionsThe current results support that the TGF-β 1 869 T>C polymorphism was associated with the risk of PE. However, the number of eligible studies is small and more studies are needed to clarify whether this association can be detected on larger sample sizes and different populations. Owing to the heterogeneity between studies, no conclusion on the association between plasma TGF-β 1 level and PE risk can be drawn from this review. Further studies about the TGF-β 1 levels at different stages of pregnancy and the development of TGF-β 1 assay methodology are required to reveal the role of TGF-β 1 in the pathological development of PE.

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“…Similar to this research, in 2006, Hu BC et al explored the association of SNPs of +869T/C of TGFB1 and EH, they also found that the +869T/C gene polymorphism of TGFB1 might be associated with EH only in women of Chinese Han population (10). In contrast to the above research, other studies in the Chinese population arrived at a complete agreement that C allele and CC genotype of TGFB1 +869T/C gene polymorphism generally increased the risk of EH in the Chinese population including both men and women (11)(12)(13)(14).…”

Section: Discussionmentioning

confidence: 82%

Transforming Growth Factor .BETA.1 +869T/C Gene Polymorphism and Essential Hypertension: A Meta-analysis Involving 2708 Participants in the Chinese Population

2011

Intern. Med.

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Background The transforming growth factor β1 (TGFB1) +869T/C gene polymorphism has been suggested to be linked to susceptibility to essential hypertension (EH). Objective and Methods To investigate the relationship between TGFB1 +869T/C gene polymorphism and EH, 5 separate studies with 2,708 subjects in the Chinese population on the relation between TGFB1 +869T/ C gene polymorphism and EH were analyzed by meta-analysis. The random effect model was selected to calculate the pooled odds ratio (ORs) and its corresponding 95% confidence interval (95%). Results There was a significant association between TGFB1 +869T/C gene polymorphism and EH. The pooled OR for CC/TC+TT genotype was 2.50 (95% CI: 1.46-4.28, P heterogeneity <0.0001, p=0.0008). The pooled OR for the frequency of C allele was 1.43 (95% CI:1.18-1.73, P heterogeneity =0.02, p=0.0002). Conclusion The current meta-analysis suggested that C allele and CC genotype of TGFB1 +869T/C gene polymorphism might be related to the increased risk of EH in the Chinese population.

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Association of TGF-β1 gene polymorphisms in exon1 and blood levels with essential hypertension

Cited by 11 publications

References 28 publications

Transforming growth factor-β and atherosclerosis: interwoven atherogenic and atheroprotective aspects

Transforming growth factor-β and atherosclerosis: interwoven atherogenic and atheroprotective aspects

Polymorphisms and Plasma Level of Transforming Growth Factor-Beta 1 and Risk for Preeclampsia: A Systematic Review

Transforming Growth Factor .BETA.1 +869T/C Gene Polymorphism and Essential Hypertension: A Meta-analysis Involving 2708 Participants in the Chinese Population

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