<i>CYP7A1</i>Gene Polymorphism Located in the 5′ Upstream Region Modifies the Risk of Coronary Artery Disease

Iwanicki, Tomasz; Balcerzyk, Anna; Niemiec, Paweł; Nowak, Tomasz; Ochalska-Tyka, Anna; Krauze, Jolanta; Kosiorz-Gorczynska, S.; Grzeszczak, W; Zak, Iwona

doi:10.1155/2015/185969

Cited by 18 publications

(16 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…(50) Reductions in CYP7A1 activity are associated with higher levels of total cholesterol (TC) and LDL, translating to an increase risk of coronary artery disease in humans, supporting this enzyme's clinical relevance. (51,52) The last step of RCT is excretion of bile acids, or cholesterol, into the bile. (43) This process is mediated by ATP-binding cassette transporter, subfamily G, member 5 (ABCG5) and member 8 (ABCG8).…”

Section: Rctmentioning

confidence: 99%

Thyroid Hormone Signaling and the Liver

2020

View full text Add to dashboard Cite

Thyroid hormone (TH) plays a critical role in maintaining metabolic homeostasis throughout life. It is well known that the liver and thyroid are intimately linked, with TH playing important roles in de novo lipogenesis, beta‐oxidation (fatty acid oxidation), cholesterol metabolism, and carbohydrate metabolism. Indeed, patients with hypothyroidism have abnormal lipid panels with higher levels of low‐density lipoprotein levels, triglycerides (triacylglycerol; TAG), and apolipoprotein B levels. Even in euthyroid patients, lower serum‐free thyroxine levels are associated with higher total cholesterol levels, LDL, and TAG levels. In addition to abnormal serum lipids, the risk of nonalcoholic fatty liver disease (NAFLD) increases with lower free thyroxine levels. As free thyroxine rises, the risk of NAFLD is reduced. This has led to numerous animal studies and clinical trials investigating TH analogs and TH receptor agonists as potential therapies for NAFLD and hyperlipidemia. Thus, TH plays an important role in maintaining hepatic homeostasis, and this continues to be an important area of study. A review of TH action and TH actions on the liver will be presented here.

show abstract

Section: Rctmentioning

confidence: 99%

Thyroid Hormone Signaling and the Liver

2020

View full text Add to dashboard Cite

show abstract

“…CYP7A1 genetic variants have been associated with defects in cholesterol and bile acid homeostasis [71]. Some of the variants are associated with higher susceptibility to cholesterol or bile acid-related human diseases, including gallbladder stone disease [72, 73], coronary artery disease [74], and biliary cirrhosis [75]. A SNP (rs3808607) in the CYP7A1 gene is also associated with a higher susceptibility to tuberculosis infection in a Moroccan population [76].…”

Section: Specific Molecular Mechanisms Of Isoniazid/rifampicin-inducementioning

confidence: 99%

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Bao

Rasmussen

et al. 2018

Curr Pharmacol Rep

View full text Add to dashboard Cite

Purpose of this Review In order to combat the development of drug resistance, the clinical treatment of tuberculosis requires the combined use of several anti-tuberculosis (anti-TB) drugs, including isoniazid and rifampicin. Combinational treatment approaches are suggested by the World Health Organization (WHO) and are widely accepted throughout the world. Unfortunately, a major side effect of the treatment is the development of anti-tuberculosis drug-induced liver injury (AT-DILI). Many factors contribute to isoniazid- and rifampicin-mediated AT-DILI and genetic variations are among the most common factors. The purpose of this review is to provide information on genetic variations associated with isoniazid- and rifampicin-mediated AT-DILI. Recent Findings The genetic variations associated with AT-DILI have been identified in the genomic regions within or near genes encoding proteins in the following pathways: drug metabolizing enzymes (NAT2, CYP2E1, and GSTs), accumulation of bile acids, lipids, and heme metabolites (CYP7A1, BSEP, UGTs, and PXR), immune adaptation (HLAs and TNF-α), and oxidant challenge (TXNRD1, SOD1, BACH1, and MAFK). Summary The information summarized in this review considers the genetic bases of risk factors contributing to AT-DILI and provides information that may help for future studies. Some of the implicated genetic variations can be used in the design of genetic tests and serve as biomarkers for the prediction of isoniazid- and rifampicin-mediated AT-DILI risk in personalized medicine.

show abstract

“…CYP7A1 belongs to the large family of P450 cytochrome proteins and is the rate-limiting enzyme during the synthesis of bile acid in the liver, which occurs through a classic pathway by producing 7-α-hydroxycholesterol (Iwanicki et al, 2015). In humans, the CYP7A1 gene is located on chromosome 8 (8q11.12) and consists of 6 exons and 5 introns (Noshiro and Okuda, 1990).…”

Section: Cyp7a1mentioning

confidence: 99%

Liver X Receptors and their Agonists: Targeting for Cholesterol Homeostasis and Cardiovascular Diseases

Ma¹,

Deng²,

Hu³

et al. 2017

Current Issues in Molecular Biology

View full text Add to dashboard Cite

Liver X receptors α (LXRα) and β (LXRβ) are essential for protection against cardiovascular diseases. LXRs are members of the nuclear receptor superfamily of DNA-binding transcription factors and act as sensors of cholesterol homeostasis. In this review, we introduce LXRs and briefly describe the roles of LXRs in reverse cholesterol transport and trans-intestinal cholesterol efflux. We discuss LXR agonists and the downstream genes of LXRs that are involved in the regulation of cholesterol transport. In addition, we describe the cardioprotective effects of LXRs against atherosclerosis, myocardial ischemia/reperfusion injury, diabetic cardiomyopathy, and myocardial hypertrophy. Finally, we expand our discussion to the actions of LXRs in atherosclerosis and suggest several potential research avenues that may be of interest to clinicians and basic scientists. The information included herein may be useful for the design of future experimental research studies and may advance the investigation of LXRs as therapeutic targets.

show abstract

CYP7A1Gene Polymorphism Located in the 5′ Upstream Region Modifies the Risk of Coronary Artery Disease

Cited by 18 publications

References 28 publications

Thyroid Hormone Signaling and the Liver

Thyroid Hormone Signaling and the Liver

Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury

Liver X Receptors and their Agonists: Targeting for Cholesterol Homeostasis and Cardiovascular Diseases

Contact Info

Product

Resources

About