G protein-coupled estrogen receptor activation by bisphenol-A disrupts lipid metabolism and induces ferroptosis in the liver

He, Wanqiu; Gao, Zhangshan; Liu, Shuhui; Tan, Lan; Wu, Yuting; Liu, Jiwen; Zheng, Zhaoqiang; Fan, Wentao; Luo, Yu; Chen, Ze‐Guo; Song, Suquan

doi:10.1016/j.envpol.2023.122211

Cited by 16 publications

(3 citation statements)

References 75 publications

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“…38 BPA was shown to bind G protein-coupled oestrogen receptor (GPER) and associated with fat accumulation in the liver of experimental animals. 39 Therefore, it appears that BPA reduces the binding of oestrogen with GPERs and thus diminishes its protective action on hepatic steatosis (Figure 2).…”

Section: B Is Phenol S Endocrine Dis Rup Tion and C Arcinog Enicit Ymentioning

confidence: 99%

Plastic compounds and liver diseases: Whether bisphenol A is the only culprit

Sangwan,

Bhattacharyya,

Banerjee

2024

Liver International

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Plastics, while providing modern conveniences, have become an inescapable source of global concern due to their role in environmental pollution. Particularly, the focus on bisphenol A (BPA) reveals its biohazardous nature and association with liver issues, specifically steatosis. However, research indicates that BPA is just one facet of the problem, as other bisphenol analogues, microplastics, nanoplastics and additional plastic derivatives also pose potential risks. Notably, BPA is implicated in every stage of non‐alcoholic fatty liver disease (NAFLD) onset and progression, surpassing hepatitis B virus as a primary cause of chronic liver disease worldwide. As plastic contamination tops the environmental contaminants list, urgent action is needed to assess causative factors and mitigate their impact. This review delves into the molecular disruptions linking plastic pollutant exposure to liver diseases, emphasizing the broader connection between plastics and the rising prevalence of NAFLD.

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Section: B Is Phenol S Endocrine Dis Rup Tion and C Arcinog Enicit Ymentioning

confidence: 99%

Plastic compounds and liver diseases: Whether bisphenol A is the only culprit

Sangwan,

Bhattacharyya,

Banerjee

2024

Liver International

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“…The discovery of selective ligands for GPER has greatly helped us to understand the physiological role of GPER. In addition, numerous synthetic estrogenic compounds have been shown to bind and/or activate GPER, including bisphenol A [ 121 , 122 , 123 , 124 ], nonylphenol [ 124 , 125 , 126 ], atrazine [ 124 , 127 , 128 ], kepone, methoxychlor, p,p’-DDT, o,p’-DDT, o,p’-DDE, p,p’-DDE, 2,2’5’-PCB-4-OH, etc. [ 17 , 124 ].…”

Section: Tissue Cellular Localization Ligands and Classical Signaling...mentioning

confidence: 99%

“…The discovery of selective ligands GPER has greatly helped us to understand the physiological role of GPER. In additio numerous synthetic estrogenic compounds have been shown to bind and/or activ GPER, including bisphenol A [121][122][123][124], nonylphenol [124][125][126], atrazine [124,127,12 kepone, methoxychlor, p,p'-DDT, o,p'-DDT, o,p'-DDE, p,p'-DDE, 2,2'5'-PCB-4-OH, e [17,124]. Lastly, there are some plant-derived polyphenols that have also been shown bind to GPER, including Genistein [124,[129][130][131], Daidzein [132], Equol [133], Oleurope [134], Hydroxytyrosol [133], Resveratrol [135][136][137], Quercetin [136,138], Tectoridin [13 Zearalenone [124,140,141], and Apigenin [136,142].…”

Section: Exogenous Ligand Of Gpermentioning

confidence: 99%

The Role of G Protein-Coupled Estrogen Receptor (GPER) in Vascular Pathology and Physiology

Xu,

Ma,

Wang

et al. 2023

Biomolecules

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Objective: Estrogen is indispensable in health and disease and mainly functions through its receptors. The protection of the cardiovascular system by estrogen and its receptors has been recognized for decades. Numerous studies with a focus on estrogen and its receptor system have been conducted to elucidate the underlying mechanism. Although nuclear estrogen receptors, including estrogen receptor-α and estrogen receptor-β, have been shown to be classical receptors that mediate genomic effects, studies now show that GPER mainly mediates rapid signaling events as well as transcriptional regulation via binding to estrogen as a membrane receptor. With the discovery of selective synthetic ligands for GPER and the utilization of GPER knockout mice, significant progress has been made in understanding the function of GPER. In this review, the tissue and cellular localizations, endogenous and exogenous ligands, and signaling pathways of GPER are systematically summarized in diverse physiological and diseased conditions. This article further emphasizes the role of GPER in vascular pathology and physiology, focusing on the latest research progress and evidence of GPER as a promising therapeutic target in hypertension, pulmonary hypertension, and atherosclerosis. Thus, selective regulation of GPER by its agonists and antagonists have the potential to be used in clinical practice for treating such diseases.

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