Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension
Both rs1801133 mutation on Methylenetetrahydrofolate reductase (MTHFR) gene and transcription factor peroxisome proliferator-activated gamma (PPARG) have been associated with plasma homocysteine (Hcy) levels and hypertension. However, their role in H-type hypertension remains unclear. In this study,...
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| Format: | Article |
| Language: | English |
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Wiley
2022-01-01
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| Series: | PPAR Research |
| Online Access: | http://dx.doi.org/10.1155/2022/2054876 |
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| author | Xiuwen Liang Tingting He Lihong Gao Libo Wei Di Rong Yu Zhang Yu Liu |
| author_facet | Xiuwen Liang Tingting He Lihong Gao Libo Wei Di Rong Yu Zhang Yu Liu |
| author_sort | Xiuwen Liang |
| collection | DOAJ |
| description | Both rs1801133 mutation on Methylenetetrahydrofolate reductase (MTHFR) gene and transcription factor peroxisome proliferator-activated gamma (PPARG) have been associated with plasma homocysteine (Hcy) levels and hypertension. However, their role in H-type hypertension remains unclear. In this study, we first tested the association between rs1801133 genotypes and Hcy level in H-type hypertension using clinical profiles collected from 203 patients before and after the treatment using enalapril maleate and folic acid tablets (EMFAT). Then, we constructed a literature-based pathway analysis to explore the role of the rs1801133-PPARG signaling pathway in H-type hypertension and its treatment. Although presented similar blood pressure, the patients with TT genotype of rs1801133 were much younger (p value <0.05) and significantly higher in Hcy levels (x2=6.11 and p<0.005) than that in the CC and CT genotype groups. Pathway analysis showed that T-allele of rs1801133 could inhibit the expression of PPARG through the downregulation of folate levels and upregulation of Hcy levels, which increased the risk of hypertension and hyperhomocysteinemia. Treatment using EMFAT led to similarly decreased Hcy levels for all patients with different genotypes (x2=86.00; p<0.36), which may occur partially through the activation of PPARG. Moreover, even after treatment, the patients with TT genotype still presented significantly higher Hcy levels (x2=7.87 and p<0.001). Our results supported that rs1801133 mutation could play a role in H-type hypertension, which might be partially through the downregulation of PPARG. Moreover, PPARG might also be involved in treating H-type hypertension using EMFAT. |
| format | Article |
| id | doaj-art-82c82e04707645d781c09914bfb7f2e9 |
| institution | Kabale University |
| issn | 1687-4765 |
| language | English |
| publishDate | 2022-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | PPAR Research |
| spelling | doaj-art-82c82e04707645d781c09914bfb7f2e92025-02-03T06:01:51ZengWileyPPAR Research1687-47652022-01-01202210.1155/2022/2054876Explore the Role of the rs1801133-PPARG Pathway in the H-type HypertensionXiuwen Liang0Tingting He1Lihong Gao2Libo Wei3Di Rong4Yu Zhang5Yu Liu6Cardiology DepartmentCardiology DepartmentNeurology DepartmentCardiology DepartmentGeriatric DepartmentCardiology DepartmentCardiology DepartmentBoth rs1801133 mutation on Methylenetetrahydrofolate reductase (MTHFR) gene and transcription factor peroxisome proliferator-activated gamma (PPARG) have been associated with plasma homocysteine (Hcy) levels and hypertension. However, their role in H-type hypertension remains unclear. In this study, we first tested the association between rs1801133 genotypes and Hcy level in H-type hypertension using clinical profiles collected from 203 patients before and after the treatment using enalapril maleate and folic acid tablets (EMFAT). Then, we constructed a literature-based pathway analysis to explore the role of the rs1801133-PPARG signaling pathway in H-type hypertension and its treatment. Although presented similar blood pressure, the patients with TT genotype of rs1801133 were much younger (p value <0.05) and significantly higher in Hcy levels (x2=6.11 and p<0.005) than that in the CC and CT genotype groups. Pathway analysis showed that T-allele of rs1801133 could inhibit the expression of PPARG through the downregulation of folate levels and upregulation of Hcy levels, which increased the risk of hypertension and hyperhomocysteinemia. Treatment using EMFAT led to similarly decreased Hcy levels for all patients with different genotypes (x2=86.00; p<0.36), which may occur partially through the activation of PPARG. Moreover, even after treatment, the patients with TT genotype still presented significantly higher Hcy levels (x2=7.87 and p<0.001). Our results supported that rs1801133 mutation could play a role in H-type hypertension, which might be partially through the downregulation of PPARG. Moreover, PPARG might also be involved in treating H-type hypertension using EMFAT.http://dx.doi.org/10.1155/2022/2054876 |
| spellingShingle | Xiuwen Liang Tingting He Lihong Gao Libo Wei Di Rong Yu Zhang Yu Liu Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension PPAR Research |
| title | Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension |
| title_full | Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension |
| title_fullStr | Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension |
| title_full_unstemmed | Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension |
| title_short | Explore the Role of the rs1801133-PPARG Pathway in the H-type Hypertension |
| title_sort | explore the role of the rs1801133 pparg pathway in the h type hypertension |
| url | http://dx.doi.org/10.1155/2022/2054876 |
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