Effects of toxicants on endoplasmic reticulum stress and hepatic cell fate determination.

Autor: Tak J; College of Pharmacy and Integrated Research Institute for Drug Development, Dongguk University-Seoul, Goyang-si, Kyeonggi-do 10326 Republic of Korea., Kim SG; College of Pharmacy and Integrated Research Institute for Drug Development, Dongguk University-Seoul, Goyang-si, Kyeonggi-do 10326 Republic of Korea.
Jazyk: angličtina
Zdroj: Toxicological research [Toxicol Res] 2023 Jul 26; Vol. 39 (4), pp. 533-547. Date of Electronic Publication: 2023 Jul 26 (Print Publication: 2023).
DOI: 10.1007/s43188-023-00201-4
Abstrakt: Toxicant-induced injury is a significant global health issue. However, the mechanisms through which toxicants such as carbon tetrachloride, acetaminophen, dimethylformamide, cocaine, and morphine induce the death of multiple cell types and contribute to liver toxicity are highly complex. This phenomenon involves intricate signaling pathways in association with oxidative stress, inflammation, and activation of death receptors, which are closely linked to endoplasmic reticulum (ER) stress. ER stress initially triggers the unfolded protein response, which either promotes cell survival or causes cell death at later times, depending on the severity and duration of the stress. Thus, comprehending the molecular basis governing cell fate determination in the context of ER stress may provide key insights into the prevention and treatment of toxicant-induced injury. This review summarizes our current understanding of agents that trigger different forms of ER stress-mediated cell death, necroptosis, ferroptosis, pyroptosis, and apoptosis, and covers the underlying molecular basis of toxicant-induced ER stress, as well as potential target molecules.
Competing Interests: Conflict of interestThe authors have no competing interests to declare.
(© The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.)
Databáze: MEDLINE
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