Targeting gap junctional intercellular communication by hepatocarcinogenic compounds

被引：4
|
作者：
Leroy, Kaat [1 ]
Pieters, Alanah [1 ]
Tabernilla, Andres [1 ]
Cooreman, Axelle [1 ]
Van Campenhout, Raf [1 ]
Cogliati, Bruno [2 ]
Vinken, Mathieu [1 ]
机构：
[1] Vrije Univ Brussel, Dept Vitro Toxicol & Dermatocosmetol, Brussels, Belgium
[2] Univ Sao Paulo, Sch Vet Med & Anim Sci, Dept Pathol, Cidade Univ, Sao Paulo, Brazil
来源：
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART B-CRITICAL REVIEWS | 2020年 / 23卷 / 06期
基金：
巴西圣保罗研究基金会;
关键词：
Connexin; gap junction intercellular communication; hepatocarcinogenicity; non-genotoxic carcinogenic compounds; risk assessment; hemichannel; in vivo; in vitro; HEPATOCELLULAR-CARCINOMA CELLS; ACTIVATED PROTEIN-KINASE; LIVER EPITHELIAL-CELLS; DI-ISONONYL PHTHALATE; BETA-OXIDATION PBOX; RAT-LIVER; CONNEXIN; 32; IN-VITRO; NONGENOTOXIC CARCINOGENS; DOWN-REGULATION;
D O I：
10.1080/10937404.2020.1781010
中图分类号：
X [环境科学、安全科学];
学科分类号：
08 ; 0830 ;
摘要：
Gap junctions in liver, as in other organs, play a critical role in tissue homeostasis. Inherently, these cellular constituents are major targets for systemic toxicity and diseases, including cancer. This review provides an overview of chemicals that compromise liver gap junctions, in particular biological toxins, organic solvents, pesticides, pharmaceuticals, peroxides, metals and phthalates. The focus in this review is placed upon the mechanistic scenarios that underlie these adverse effects. Further, the potential use of gap junctional activity as anin vitrobiomarker to identify non-genotoxic hepatocarcinogenic chemicals is discussed.
引用
收藏
页码：255 / 275
页数：21
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