Association between heme oxygenase-1 gene promoter polymorphisms and metabolic syndrome in Iranians

Javanmard, Shaghayegh Haghjooy; Keyhanian, Kiandokht; Loghmani, Parisa; Samety, Amir Abbas; Haghdoost, Faraidoon; Rafiei, Laleh; Talaei, Mohammad; Asgari, Soheila; Jazi, Mohammad Hashemi; Sarrafzadegan, Nizal

doi:10.1007/s11033-011-1105-7

Cited by 6 publications

(4 citation statements)

References 19 publications

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“…HO-1 participates in iron homeostasis. Javanmard et al [42] generated mice with targeted HO-1 null mutations and analyzed parameters of iron metabolism and they discovered that adult HO-1-deficient animals develop both serum iron deficiency and pathological iron-loading, indicating that HO-1 is crucial for the expulsion of iron from tissue stores.…”

Section: Mechanisms Of Action Of Hmox-1 In the Livermentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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The activation of heme oxygenase-1 (HO-1) appears to be an endogenous defensive mechanism used by cells to reduce inflammation and tissue damage in a number of injury models. HO-1, a stress-responsive enzyme that catabolizes heme into carbon monoxide (CO), biliverdin and iron, has previously been shown to protect grafts from ischemia/reperfusion and rejection. In addition, the products of the HO-catalyzed reaction, particularly CO and biliverdin/bilirubin, have been shown to exert protective effects in the liver against a number of stimuli, as in chronic hepatitis C and in transplanted liver grafts. Furthermore, the induction of HO-1 expression can protect the liver against damage caused by a number of chemical compounds. More specifically, the CO derived from HO-1-mediated heme catabolism has been shown to be involved in the regulation of inflammation; furthermore, administration of REVIEW 541October 27, 2013|Volume 5|Issue 10| WJH|www.wjgnet.com low concentrations of exogenous CO has a protective effect against inflammation. Both murine and human HO-1 deficiencies have systemic manifestations associated with iron metabolism, such as hepatic overload (with signs of a chronic hepatitis) and iron deficiency anemia (with paradoxical increased levels of ferritin). Hypoxia induces HO-1 expression in multiple rodent, bovine and monkey cell lines, but interestingly, hypoxia represses expression of the human HO-1 gene in a variety of human cell types (endothelial cells, epithelial cells, T cells). These data suggest that HO-1 and CO are promising novel therapeutic molecules for patients with inflammatory diseases. In this review, we present what is currently known regarding the role of HO-1 in liver injuries and in particular, we focus on the implications of targeted induction of HO-1 as a potential therapeutic strategy to protect the liver against chemically induced injury.

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Section: Mechanisms Of Action Of Hmox-1 In the Livermentioning

confidence: 99%

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Origassa¹,

Câmara²

2013

WJH

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“…Studies relating haeme oxygenase pathway activity to clinical phenotypes and outcomes in humans AA SNP is associated with increased risk of hypertension in women148 and in individuals with MetS 151 † Shorter GT repeats/greater HO-1 expression is associated with lower diastolic blood pressure,151 lower systolic blood pressure and less hypertension 152 † HO-1 promoter SNPs associated with hypertension149 † Longer GT repeats/lower HO-1 expression is associated with lower risk of essential hypertension150 No difference in promoter length or allelic frequency between MetS and controls,153 or between T2DM, MetS, and controls154 but S/M genotype was increased in T2DM and MetS patients compared with controls154 …”

mentioning

confidence: 99%

Haeme oxygenase signalling pathway: implications for cardiovascular disease

2015

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Evidence now points to the haeme oxygenase (HO) pathway as a possible actor in modulating risk for cardiovascular disease (CVD). In particular, the HO pathway may represent a key endogenous modulator of oxidative, inflammatory, and cytotoxic stress while also exhibiting vasoregulatory properties. In this review, we summarize the accumulating experimental and emerging clinical data indicating how activity of the HO pathway and its products may play a role in mechanisms underlying the development of CVD. We also identify gaps in the literature to date and suggest future directions for investigation. Because HO pathway activity can be influenced not only by genetic traits and environmental stimuli but also by a variety of existing pharmacologic interventions, the pathway could serve as a prime target for reducing the overall burden of CVD. Further work is needed to determine the role of HO pathway products as possible prognostic markers of risk for clinical CVD events and the extent to which therapeutic augmentation or inhibition of HO pathway activity could serve to modify CVD risk.

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“…Polymorphisms in HMOX1 and NQO1 have been associated with several oxidative stress-related diseases, including cancer, diabetes, and Alzheimer’s disease [ 9 , 10 , 14 – 17 ]. MetS is an important public health issue.…”

Section: Discussionmentioning

confidence: 99%

“…The Keap1/Nrf2/ARE pathway plays a central role in regulating the expressions of genes that are crucial mediators of cellular defence against oxidative stress and chronic inflammation such as the HMOX1 gene that encodes heme oxygenase 1 (HO-1) and the NQO1 gene that encodes NADPH-quinone oxidoreductase 1 [ 9 , 10 ]. Polymorphisms in these genes can affect their antioxidant functions.…”

Section: Introductionmentioning

confidence: 99%

Association of HMOX1 and NQO1 Polymorphisms with Metabolic Syndrome Components

et al. 2015

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Metabolic syndrome (MetS) is among the most important public health problems worldwide, and is recognized as a major risk factor for various illnesses, including type 2 diabetes mellitus, obesity, and cardiovascular diseases. Recently, oxidative stress has been suggested as part of MetS aetiology. The heme oxygenase 1 (HMOX1) and NADH:quinone oxidoreductase 1 (NQO1) genes are crucial mediators of cellular defence against oxidative stress. In the present study, we analysed the associations of HMOX1 (GT)n and NQO1 C609T polymorphisms with MetS and its components. Our study population comprised 735 Mexican Mestizos unrelated volunteers recruited from different tertiary health institutions from Mexico City. In order to know the HMOX1 (GT)n and NQO1 C609T allele frequencies in Amerindians, we included a population of 241 Amerindian native speakers. Their clinical and demographic data were recorded. The HMOX1 (GT)n polymorphism was genotyped using PCR and fluorescence technology. NQO1 C609T polymorphism genotyping was performed using TaqMan probes. Short allele (<25 GT repeats) of the HMOX1 polymorphism was associated with high systolic and diastolic blood pressure, and the T allele of the NQO1 C609T polymorphism was associated with increased triglyceride levels and decreased HDL-c levels, but only in individuals with MetS. This is the first study to analyse the association between MetS and genes involved in oxidative stress among Mexican Mestizos. Our data suggest that polymorphisms of HMOX1 and NQO1 genes are associated with a high risk of metabolic disorders, including high systolic and diastolic blood pressure, hypertriglyceridemia, and low HDL-c levels in Mexican Mestizo individuals.

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Association between heme oxygenase-1 gene promoter polymorphisms and metabolic syndrome in Iranians

Cited by 6 publications

References 19 publications

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Cytoprotective role of heme oxygenase-1 and heme degradation derived end products in liver injury

Haeme oxygenase signalling pathway: implications for cardiovascular disease

Association of HMOX1 and NQO1 Polymorphisms with Metabolic Syndrome Components

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