ABCG8

Last update 08 May 2025

Basic Info

Synonyms

ABCG8, ATP binding cassette subfamily G member 8, ATP-binding cassette sub-family G member 8

+ [6]

Introduction

ABCG5 and ABCG8 form an obligate heterodimer that mediates Mg(2+)- and ATP-dependent sterol transport across the cell membrane. Plays an essential role in the selective transport of the dietary cholesterol in and out of the enterocytes and in the selective sterol excretion by the liver into bile (PubMed:11099417, PubMed:11452359, PubMed:15054092, PubMed:27144356). Required for normal sterol homeostasis (PubMed:11099417, PubMed:11452359, PubMed:15054092). The heterodimer with ABCG5 has ATPase activity (PubMed:16893193, PubMed:20210363, PubMed:27144356).

100 Clinical Results associated with ABCG8

100 Translational Medicine associated with ABCG8

0 Patents (Medical) associated with ABCG8

719

Literatures (Medical) associated with ABCG8

01 Jun 2025·Phytomedicine

Protective effects of albiflorin on acetaminophen-induced hepatotoxicity: Regulation of blood–biliary barrier integrity by ATF3

Article

Author: Zhao, Yan ; Zhai, Xiaohan ; Wang, Yue ; Hu, Yan ; Wang, Zhecheng ; Lin, Musen ; Lv, Li ; Yao, Jihong ; Luan, Qinrong

BACKGROUNDAcetaminophen-induced hepatotoxicity remains a clinical challenge with limited targeted therapeutic options. While recent advances have identified blood‒biliary barrier disruption as a critical pathogenic mechanism, effective interventions preserving this barrier are notably lacking. Albiflorin, a key bioactive constituent of Paeonia lactiflora Pall., exhibits unique bile acid modulation along with antioxidant and anti-inflammatory activities, suggesting its potential efficacy in preventing acetaminophen-induced liver injury. However, its specific role and underlying mechanisms in alleviating acetaminophen-induced hepatotoxicity remain unclear.OBJECTIVEThis study's objective was to examine the pharmacological effects and primary molecular mechanisms of albiflorin in alleviating acetaminophen-induced liver injury.METHODSAn acetaminophen-induced liver injury mouse model was created using a 300 mg/kg dose of acetaminophen. The hepatoprotective effects of albiflorin were assessed through histological and biochemical analyses. Blood‒biliary barrier integrity was evaluated via Evans blue dye tests, immunofluorescence, and bile acid assays. Transcriptomic analysis, gene overexpression and interference techniques, and ChIP‒qPCR were employed to explore the molecular mechanisms underlying the protective effects of albiflorin.RESULTSAlbiflorin significantly reduced acetaminophen-induced liver injury, as evidenced by improved biochemical profiles and hepatocyte morphology. It also prevented increases in blood‒biliary barrier permeability and bile acid levels. RNA sequencing identified 3,184 differentially expressed genes, revealing critical pathways involved in maintaining blood‒biliary barrier integrity. AF reversed the acetaminophen-induced changes in the expression of genes related to the blood‒biliary barrier, particularly occludin, claudin 5, ABCG5, and ABCG8. Albiflorin protected the blood‒biliary barrier and mitigated acetaminophen-induced liver injury by enhancing ATF3 protein stability, with ATF3 identified as a critical mediator of these protective effects.CONCLUSIONThis study provides pioneering evidence that albiflorin protects against acetaminophen-induced liver injury by interacting with ATF3 to regulate blood-biliary barrier proteins and maintain the integrity of the blood-biliary barrier. These findings deepen our understanding of the role of the blood‒biliary barrier in liver diseases and suggest a therapeutic strategy for drug overdose-induced liver injury.

01 Jun 2025·Toxicology Reports

Effects of opium on cholesterol metabolism in rats fed normal and high-fat/high-cholesterol diet

Article

Author: Abbasi, Ebrahim ; Khodadadi, Iraj ; Shafiee, Gholamreza ; Ebrahimi, Elaheh

There is a misconception that opium can lower blood sugar and cholesterol levels. Hence, this study aimed to investigate the influences of opium on the expression of key cholesterol metabolism genes in the liver and intestine of rats receiving a cholesterol-rich diet. Male Wistar rats were randomly divided into four groups (n = 6): normal control, opium addiction, hypercholesterolemic diet, and opium addiction received hypercholesterolemic diet. After 28 days, the blood glucose levels, liver enzymes, and cholesterol in the rat's serum were measured. The cholesterol regulatory genes and transporters such as 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, low-density lipoprotein receptor (LDL-R), cholesterol 7 alpha-hydroxylase 1 (CYP7A1) (in liver tissue), and ATP Binding cassette subfamily g member 5 and 8 (ABCG5 and ABCG8), and Niemann-Pick C1-like 1 protein (NPC1L1) (in intestinal tissue) were measured. Intestinal morphological changes were also evaluated. Opium decreased serum glucose and total cholesterol levels (P < 0.05). In contrast, the levels of liver enzymes increased compared to the normal control group (P < 0.05). Histological examinations revealed that opium caused disorganization, deformation, and destruction of cells in intestinal tissue. Real-time PCR analysis demonstrated that opium increased the expression of LDL receptor genes, HMG-CoA reductase enzyme, and CYP7A1 in the liver compared to the normal control group (P < 0.05). The changes of ABCG8 and NPC1L1 transporters in intestinal tissue were not significant. Opium had beneficial effects on blood lipid and glucose levels, but histological findings indicated destructive effects on intestinal tissues.

25 Apr 2025·Circulation Research

MAIT Cells Promote Cholesterol Excretion Pathways Mitigating Atherosclerosis

Article

Author: Haas, Joel T. ; Lhomme, Marie ; Galier, Sophie ; Lehuen, Agnès ; Wang, Hua ; Zhang, Kaidi ; Ichou, Farid ; Materne, Clément ; Salem, Joe-Elie ; Kc, Pukar ; Neves, Carolina ; Lesnik, Philippe ; Guerin, Maryse

BACKGROUND:Previous clinical studies have indicated reduced circulating mucosal-associated invariant T (MAIT) cells in individuals with coronary artery disease. However, the precise role and underlying mechanisms of MAIT cells in this context remain unclear. Immune homeostasis plays a pivotal role in the development of atherosclerosis. This study explores the impact of MAIT cells on atherosclerosis.METHODS: Vα19 +/− Ldlr −/− mice, characterized by a high MAIT cell frequency, and MAIT cell deficient MR1 −/− (major histocompatibility complex-related molecule 1) Ldlr −/− mice and their respective controls were used. Starting at 6 weeks of age, mice were subjected to a 1% cholesterol diet for 16 weeks. Additionally, the study analyzed circulating MAIT cell frequency and cholesterol levels in 68 patients with hypercholesterolemia. RESULTS: In Vα19 +/− Ldlr −/− mice, increased MAIT cells demonstrated a protective effect against atherosclerosis by reducing VLDL-C (very-low-density lipoprotein cholesterol) levels through heightened cholesterol excretion. This effect was accompanied by elevated jejunal ABCB1a, ABCG5, and ABCG8 expression, mediated by augmented levels of Liver X receptor transcription and activation, likely through intestinal IL-22 (interleukin-22) signaling. Conversely, cholesterol reduction mediated by intestinal cholesterol excretion was blocked by inhibition of MAIT cells. Moreover, MAIT cell-deficient MR1 −/− Ldlr −/− mice exhibited elevated total cholesterol levels and increased atherosclerotic lesions. In patients with hypercholesterolemia, circulating MAIT cell frequency displayed negative correlations with VLDL-C levels and positive correlations with HDL-C (high-density lipoprotein cholesterol) levels. CONCLUSIONS:Our findings demonstrate a new mechanism for plasma VLDL-C clearance by MAIT cell-mediated cholesterol excretion. The results provide further evidence that immunity is involved in cholesterol homeostasis. Targeting intestinal immunity to regulate cholesterol homeostasis holds promise as a new cholesterol-lowering modality to prevent atherosclerotic cardiovascular disease.

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ABCG8

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