Flame Retardants-Mediated Interferon Signaling in the Pathogenesis of Nonalcoholic Fatty Liver Disease

International Journal of Molecular Sciences

Hubert Dirven¹  Sabbir Khan²  Luděk Bláha³  ChanderK. Negi³  Lola Bajard³ 

[1] Department of Environmental Health, Section for Toxicology and Risk Assessment, Norwegian Institute of Public Health, 0456 Oslo, Norway;Department of Neuro-Oncology, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA;Faculty of Science, RECETOX, Masaryk University, Kamenice 5, CZ62500 Brno, Czech Republic;

关键词: flame retardants;    nonalcoholic fatty liver disease;    metabolism-disrupting chemicals;    cytokines;    interferon;    metabolic disruption;   

DOI  :  10.3390/ijms22084282

来源: DOAJ

【 摘 要 】

Nonalcoholic fatty liver disease (NAFLD) is a growing concern worldwide, affecting 25% of the global population. NAFLD is a multifactorial disease with a broad spectrum of pathology includes steatosis, which gradually progresses to a more severe condition such as nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually leads to hepatic cancer. Several risk factors, including exposure to environmental toxicants, are involved in the development and progression of NAFLD. Environmental factors may promote the development and progression of NAFLD by various biological alterations, including mitochondrial dysfunction, reactive oxygen species production, nuclear receptors dysregulation, and interference in inflammatory and immune-mediated signaling. Moreover, environmental contaminants can influence immune responses by impairing the immune system’s components and, ultimately, disease susceptibility. Flame retardants (FRs) are anthropogenic chemicals or mixtures that are being used to inhibit or delay the spread of fire. FRs have been employed in several household and outdoor products; therefore, human exposure is unavoidable. In this review, we summarized the potential mechanisms of FRs-associated immune and inflammatory signaling and their possible contribution to the development and progression of NAFLD, with an emphasis on FRs-mediated interferon signaling. Knowledge gaps are identified, and emerging pharmacotherapeutic molecules targeting the immune and inflammatory signaling for NAFLD are also discussed.

【 授权许可】

Unknown