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Drug-Induced Liver Injury (DILIN) GWAS

ABSTRACT: Drug-Induced Liver Injury (DILIN) GWAS

PROVIDER: PRJNA219213 | ENA |

REPOSITORIES: ENA

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NIDDK Drug-Induced Liver Injury Network (DILIN)

Project description:<p>The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) has established the Drug-Induced Liver Injury Network (DILIN) to collect and analyze cases of severe liver injury caused by prescription drugs, over-the-counter drugs, and alternative medicines, such as herbal products and supplements.</p>

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Small RNAs in anti-tuberculosis drug-induced liver injury

Project description:The antimicrobials isoniazid and pyrazinamide, used for the treatment of tuberculosis are known to cause drug-induced liver injury in humans. This limits the effectiveness of tuberculosis treatment, resulting in incomplete cure, relapse and the development of antimicrobial resistance. MicroRNAs are known to be good biomarkers of disease, with the microRNA miR-122 being diagnostic for liver injury. In this study zebrafish larvae were exposed to the anti-tuberculosis drugs isoniazid and pyrazinamide at concentrations which demonstrated liver injury by microscopy and histology. The aim of this study is to understand small RNA changes occurring in anti-tuberculosis drug-induced liver injury and to attempt to identify novel microRNA biomarkers of liver injury.

2023-12-25 | GSE146260 | GEO

Small RNAs in anti-tuberculosis drug-induced liver injury

Project description:Small RNAs in anti-tuberculosis drug-induced liver injury

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The role of corticosterone in nevirapine-induced idiosyncratic drug-induced liver injury

Project description:Nevirapine, an antiretroviral used in the treatment of HIV, is associated with idiosyncratic drug-induced liver injury (IDILI), a potentially life-threatening adverse drug reaction. Its usage has decreased due to this concern, but it is still widely used in lower-resource settings. In general, the mechanisms underlying idiosyncratic drug reactions (IDRs) are poorly understood, but evidence indicates that most are immune-mediated. There is very limited understanding of the early immune response following administration of drugs associated with IDRs, which likely occurs due to reactive metabolite formation. In this work, we aimed to characterize the links between covalent binding of nevirapine, the development of an early immune response, and the subsequent liver injury using a mouse model. We describe initial attempts to characterize an early immune response to nevirapine followed by the discovery that nevirapine induced the release of corticosterone. Corticosterone release was partially associated with the degree of drug covalent binding in the liver, but was also likely mediated by additional mechanisms at higher drug doses. Transcriptomic analysis confirmed metabolic activation, glucocorticoid signaling, and decreased immune activation; GDF-15 also warrants further investigation as part of the immune response to nevirapine. Finally, glucocorticoid blockade preceding the first dose of nevirapine attenuated nevirapine-induced liver injury at 3 weeks, suggesting that acute glucocorticoid signaling is harmful in the context of nevirapine-induced liver injury. This work demonstrates that nevirapine induces acute corticosterone release, which contributes to delayed-onset liver injury. It also has implications for screening drug candidates for IDILI risk and preventing nevirapine-induced IDILI.

2024-04-15 | GSE255038 | GEO

Proteomic-based identification of APCS as candidate protein for diagnosis of patients exhibiting Anti-tubercular drug induced liver injury

Project description:In the present study, the proteomics approach identified potential protein signatures with high discriminative ability in TB patients with and without drug-induced liver injury which might play a crucial role in developing Anti-tubercular drug-induced liver injury.

2021-11-12 | MSV000088373 | MassIVE

The role of corticosterone in nevirapine-induced idiosyncratic drug-induced liver injury

Project description:The role of corticosterone in nevirapine-induced idiosyncratic drug-induced liver injury

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Polygenic architecture informs potential vulnerability to drug-induced liver injury

Project description:Polygenic architecture informs potential vulnerability to drug-induced liver injury

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Hepatic p53 protein level governs liver s sensitivity to drug-induced liver injury

Project description:Hepatic p53 protein level governs liver s sensitivity to drug-induced liver injury

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Knockdown of PPARγ can ameliorate benzbromarone-induced obesity-specific drug-induced liver injury

Project description:Objective: Benzbromarone (BBR) is an effective uric acid-lowering drug. However, it can induce severe liver damage in some patients. Studies have shown that BBR specifically exacerbates hepatic steatosis in obese individuals, leading to aggravated liver injury. The exact mechanism behind this phenomenon remains unclear. Methods: db/db mice were divided into four groups: Control, BBR administration (BBR), Pparg knockdown (Pparg-KD), and BBR administration with Pparg knockdown (BBR + Pparg-KD). One week after AAV8-shRNA-Pparg virus injection, mice were orally administered BBR for four weeks, and changes in blood glucose and body weight were measured. Subsequently, samples were collected, and plasma lipid levels, hepatic lipid content, and liver function parameters were determined. RNA-seq was performed to assess changes in the hepatic gene expression profile and analyze the protective effect of PPARγ knockdown on BBR-induced drug-induced liver injury. Results: Mice in the BBR group exhibited more severe levels of plasma lipids, hepatic lipids, and liver function parameters compared to the Control group. However, mice in the BBR + Pparg-KD group showed significant improvements in these indicators compared to the BBR group. Transcriptomic analysis revealed that BBR administration upregulated the expression of various lipid synthesis-related genes, primarily associated with the PPAR signaling pathway. Furthermore, PPARγ knockdown reversed the increased expression of these lipid synthesis genes. This suggests that PPARγ knockdown has a significant protective effect against BBR-induced drug-induced liver injury. Conclusion: Hepatocyte-specific knockdown of PPARγ can protect against BBR-induced exacerbation of hepatic steatosis and liver injury by inhibiting the promotion of lipid synthesis through PPARγ activation.

2025-01-29 | GSE274748 | GEO

Knockdown of PPARγ can ameliorate benzbromarone-induced obesity-specific drug-induced liver injury

Project description:Knockdown of PPARγ can ameliorate benzbromarone-induced obesity-specific drug-induced liver injury

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