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TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α

Impairment of liver regeneration leads to severe morbidity in acute and chronic severe liver disease. Transient receptor potential melastain 8 (TRPM8) is involved in a variety of processes, including temperature sensing, ion homeostasis, and cell proliferation. However, whether TRPM8 contributes to...

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Autores principales: Lei, Xiaohua, Liu, Qiang, Qin, Wei, Tong, Qing, Li, Zhenghao, Xu, Wendi, Liu, Guoxing, Fu, Jie, Zhang, Ju, Kuang, Tao, Shao, Yaoli, Liu, Chun, Fang, Yu, Cao, Zhenyu, Yan, Likun, Liu, Zhiqiang, Liu, Siyuan, Yamamoto, Hirofumi, Mori, Masaki, Liang, Xin M., Xu, Xundi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9758188/
https://www.ncbi.nlm.nih.gov/pubmed/36526620
http://dx.doi.org/10.1038/s41419-022-05475-4
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author Lei, Xiaohua
Liu, Qiang
Qin, Wei
Tong, Qing
Li, Zhenghao
Xu, Wendi
Liu, Guoxing
Fu, Jie
Zhang, Ju
Kuang, Tao
Shao, Yaoli
Liu, Chun
Fang, Yu
Cao, Zhenyu
Yan, Likun
Liu, Zhiqiang
Liu, Siyuan
Yamamoto, Hirofumi
Mori, Masaki
Liang, Xin M.
Xu, Xundi
author_facet Lei, Xiaohua
Liu, Qiang
Qin, Wei
Tong, Qing
Li, Zhenghao
Xu, Wendi
Liu, Guoxing
Fu, Jie
Zhang, Ju
Kuang, Tao
Shao, Yaoli
Liu, Chun
Fang, Yu
Cao, Zhenyu
Yan, Likun
Liu, Zhiqiang
Liu, Siyuan
Yamamoto, Hirofumi
Mori, Masaki
Liang, Xin M.
Xu, Xundi
author_sort Lei, Xiaohua
collection PubMed
description Impairment of liver regeneration leads to severe morbidity in acute and chronic severe liver disease. Transient receptor potential melastain 8 (TRPM8) is involved in a variety of processes, including temperature sensing, ion homeostasis, and cell proliferation. However, whether TRPM8 contributes to liver regeneration is still unclear. We assessed the effect and mechanism of TRPM8 in liver regeneration and hepatocyte proliferation in vivo and in vitro. In this study, we found that TRPM8 deficiency impairs liver regeneration in mice. Mechanistically, the results revealed that mitochondrial energy metabolism was attenuated in livers from TRPM8 knockout (KO) mice. Furthermore, we found that TRPM8 contributes to the proliferation of hepatocytes via PGC1α. Taken together, this study shows that TRPM8 contributes to liver regeneration in mice after hepatectomy. Genetic approaches and pharmacological approaches to regulate TRPM8 activity may be beneficial to the promotion of liver regeneration. [Image: see text]
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spelling pubmed-97581882022-12-18 TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α Lei, Xiaohua Liu, Qiang Qin, Wei Tong, Qing Li, Zhenghao Xu, Wendi Liu, Guoxing Fu, Jie Zhang, Ju Kuang, Tao Shao, Yaoli Liu, Chun Fang, Yu Cao, Zhenyu Yan, Likun Liu, Zhiqiang Liu, Siyuan Yamamoto, Hirofumi Mori, Masaki Liang, Xin M. Xu, Xundi Cell Death Dis Article Impairment of liver regeneration leads to severe morbidity in acute and chronic severe liver disease. Transient receptor potential melastain 8 (TRPM8) is involved in a variety of processes, including temperature sensing, ion homeostasis, and cell proliferation. However, whether TRPM8 contributes to liver regeneration is still unclear. We assessed the effect and mechanism of TRPM8 in liver regeneration and hepatocyte proliferation in vivo and in vitro. In this study, we found that TRPM8 deficiency impairs liver regeneration in mice. Mechanistically, the results revealed that mitochondrial energy metabolism was attenuated in livers from TRPM8 knockout (KO) mice. Furthermore, we found that TRPM8 contributes to the proliferation of hepatocytes via PGC1α. Taken together, this study shows that TRPM8 contributes to liver regeneration in mice after hepatectomy. Genetic approaches and pharmacological approaches to regulate TRPM8 activity may be beneficial to the promotion of liver regeneration. [Image: see text] Nature Publishing Group UK 2022-12-16 /pmc/articles/PMC9758188/ /pubmed/36526620 http://dx.doi.org/10.1038/s41419-022-05475-4 Text en © The Author(s) 2023, corrected publication 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Article
Lei, Xiaohua
Liu, Qiang
Qin, Wei
Tong, Qing
Li, Zhenghao
Xu, Wendi
Liu, Guoxing
Fu, Jie
Zhang, Ju
Kuang, Tao
Shao, Yaoli
Liu, Chun
Fang, Yu
Cao, Zhenyu
Yan, Likun
Liu, Zhiqiang
Liu, Siyuan
Yamamoto, Hirofumi
Mori, Masaki
Liang, Xin M.
Xu, Xundi
TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α
title TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α
title_full TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α
title_fullStr TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α
title_full_unstemmed TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α
title_short TRPM8 contributes to liver regeneration via mitochondrial energy metabolism mediated by PGC1α
title_sort trpm8 contributes to liver regeneration via mitochondrial energy metabolism mediated by pgc1α
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9758188/
https://www.ncbi.nlm.nih.gov/pubmed/36526620
http://dx.doi.org/10.1038/s41419-022-05475-4
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