Version 1
: Received: 26 April 2017 / Approved: 26 April 2017 / Online: 26 April 2017 (17:57:38 CEST)
How to cite:
Yamada, S.; Guo, X.; Tanimoto, A. Peroxiredoxin 4 (PRDX4): Its Critical In Vivo Roles in Animal Models of Metabolic Syndrome Using Our Unique PRDX4 Transgenic Mice. Preprints2017, 2017040171. https://doi.org/10.20944/preprints201704.0171.v1
Yamada, S.; Guo, X.; Tanimoto, A. Peroxiredoxin 4 (PRDX4): Its Critical In Vivo Roles in Animal Models of Metabolic Syndrome Using Our Unique PRDX4 Transgenic Mice. Preprints 2017, 2017040171. https://doi.org/10.20944/preprints201704.0171.v1
Yamada, S.; Guo, X.; Tanimoto, A. Peroxiredoxin 4 (PRDX4): Its Critical In Vivo Roles in Animal Models of Metabolic Syndrome Using Our Unique PRDX4 Transgenic Mice. Preprints2017, 2017040171. https://doi.org/10.20944/preprints201704.0171.v1
APA Style
Yamada, S., Guo, X., & Tanimoto, A. (2017). Peroxiredoxin 4 (PRDX4): Its Critical <em>In Vivo</em> Roles in Animal Models of Metabolic Syndrome Using Our Unique PRDX4 Transgenic Mice. Preprints. https://doi.org/10.20944/preprints201704.0171.v1
Chicago/Turabian Style
Yamada, S., Xin Guo and Akihide Tanimoto. 2017 "Peroxiredoxin 4 (PRDX4): Its Critical <em>In Vivo</em> Roles in Animal Models of Metabolic Syndrome Using Our Unique PRDX4 Transgenic Mice" Preprints. https://doi.org/10.20944/preprints201704.0171.v1
Abstract
The peroxiredoxin (PRDX) family, a new family of proteins with a pivotal antioxidative function, is ubiquitously synthesized and abundantly identified in various organisms. In contrast to the intracellular localization of other family members (PRDX1/2/3/5/6), PRDX4 is the only known secretory form and protects against oxidative damage by scavenging reactive oxygen species in both the intracellular (especially the endoplasmic reticulum) compartments and the extracellular space. Recently, we generated unique human PRDX4 (hPRDX4) transgenic (Tg) mice on a C57BL/6J background and investigated the critical and diverse protective roles of PRDX4 against diabetes mellitus, atherosclerosis, insulin resistance, and nonalcoholic fatty liver disease (NAFLD) as well as evaluated its role in the intestinal function in various animal models. Our published data have shown that PRDX4 helps prevent the progression of metabolic syndrome by reducing local and systemic oxidative stress and synergistically suppressing steatosis, inflammatory reactions, and/or apoptotic activity. These observations suggest that Tg mice may be a useful animal model for studying the relevance of oxidative stress on inflammation and the dysregulation of lipid/bile acid/glucose metabolism upon the progression of human metabolic syndrome, and that specific accelerators of PRDX4 may be useful as therapeutic agents for ameliorating various chronic inflammatory diseases.
Biology and Life Sciences, Endocrinology and Metabolism
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
