TY - JOUR
T1 - Carbon monoxide-triggered health effects
T2 - the important role of the inflammasome and its possible crosstalk with autophagy and exosomes
AU - Chen, Rong Jane
AU - Lee, Yu-Hsuan
AU - Chen, Tzu Hao
AU - Chen, Yu Ying
AU - Yeh, Ya Ling
AU - Chang, Ching Ping
AU - Huang, Chien Cheng
AU - Guo, How Ran
AU - Wang, Ying Jan
N1 - Funding Information:
This work was supported by the Ministry of Science and Technology, Taiwan through Grants MOST 108-2638-B-006-001-MY2, MOST 107-2311-B-006-004-MY3, MOST 108-2314-B-384-010, MOST 109-2314-B-384-005-MY3, MOST 108-2314-B-039-061?MY3, MOST 109-2314-B-006-051-MY3, and MOST 108-2314-B-006-057. Figure 1 were created using BioRender.com.
Publisher Copyright:
© 2021, The Author(s), under exclusive licence to Springer-Verlag GmbH, DE part of Springer Nature.
PY - 2021/4
Y1 - 2021/4
N2 - Carbon monoxide (CO) has long been known as a “silent killer” because of its ability to bind hemoglobin (Hb), leading to reduced oxygen carrying capacity of Hb, which is the main cause of CO poisoning (COP) in humans. Emerging studies suggest that mitochondria is a key target of CO action that can impact key biological processes, including apoptosis, cellular proliferation, inflammation, and autophagy. Despite its toxicity at high concentrations, CO also exhibits cyto- and tissue-protective effects at low concentrations in animal models of organ injury and disease. Specifically, CO modulates the production of pro- or anti-inflammatory cytokines and mediators by regulating the NLRP3 inflammasome. Given that human diseases are strongly associated with inflammation, a deep understanding of the exact mechanism is helpful for treatment. Autophagic factors and inflammasomes interact in various situations, including inflammatory disease, and exosomes might function as the bridge between the inflammasome and autophagy activation. Thus, the interplay among autophagy, mitochondrial dysfunction, exosomes, and the inflammasome may play pivotal roles in the health effects of CO. In this review, we summarize the latest research on the beneficial and toxic effects of CO and their underlying mechanisms, focusing on the important role of the inflammasome and its possible crosstalk with autophagy and exosomes. This knowledge may lead to the development of new therapies for inflammation-related diseases and is essential for the development of new therapeutic strategies and biomarkers of COP.
AB - Carbon monoxide (CO) has long been known as a “silent killer” because of its ability to bind hemoglobin (Hb), leading to reduced oxygen carrying capacity of Hb, which is the main cause of CO poisoning (COP) in humans. Emerging studies suggest that mitochondria is a key target of CO action that can impact key biological processes, including apoptosis, cellular proliferation, inflammation, and autophagy. Despite its toxicity at high concentrations, CO also exhibits cyto- and tissue-protective effects at low concentrations in animal models of organ injury and disease. Specifically, CO modulates the production of pro- or anti-inflammatory cytokines and mediators by regulating the NLRP3 inflammasome. Given that human diseases are strongly associated with inflammation, a deep understanding of the exact mechanism is helpful for treatment. Autophagic factors and inflammasomes interact in various situations, including inflammatory disease, and exosomes might function as the bridge between the inflammasome and autophagy activation. Thus, the interplay among autophagy, mitochondrial dysfunction, exosomes, and the inflammasome may play pivotal roles in the health effects of CO. In this review, we summarize the latest research on the beneficial and toxic effects of CO and their underlying mechanisms, focusing on the important role of the inflammasome and its possible crosstalk with autophagy and exosomes. This knowledge may lead to the development of new therapies for inflammation-related diseases and is essential for the development of new therapeutic strategies and biomarkers of COP.
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U2 - 10.1007/s00204-021-02976-7
DO - 10.1007/s00204-021-02976-7
M3 - Review article
C2 - 33554280
AN - SCOPUS:85100528293
VL - 95
SP - 1141
EP - 1159
JO - Archiv fur Toxikologie
JF - Archiv fur Toxikologie
SN - 0003-9446
IS - 4
ER -