Evidence map›Paper›PMID 35525986›Full record

ArticleCell & bioscience2022

TRPM8 deficiency attenuates liver fibrosis through S100A9-HNF4α signaling.

Qiang Liu, Xiaohua Lei, Zhenyu Cao, Ju Zhang, Likun Yan, Jie Fu, Qing Tong, Wei Qin, Yaoli Shao, Chun Liu and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Role of TRP Channels in Liver-Related Diseases.International journal of molecular sciences · 2023
    Review
  8. Programmed Cell Death in Liver Fibrosis.Journal of inflammation research · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 5 institutions in 3 countries.

Qiang LiuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Xiaohua LeiHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Zhenyu CaoHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Ju ZhangHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Likun YanHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Jie FuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Qing TongHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Wei QinHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Yaoli ShaoHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Chun LiuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Zhiqiang LiuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Zicheng WangHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Yuan ChuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Ge XuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Siyuan LiuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Xueyi WenHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China.
Hirofumi YamamotoDepartment of Surgery and Clinical Oncology, Graduate School of Medicine, Osaka University, Suita City, Osaka, 565-0871, Japan.
Masaki MoriDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, 812-8582, Japan.
Xin M LiangWellman Center for Photomedicine, Division of Hematology and Oncology, Division of Endocrinology, Massachusetts General Hospital, VA Boston Healthcare System, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, 02115, USA. xin.m.liang.phd@gmail.com.
Xundi XuHunan Provincial Key Laboratory of Hepatobiliary Disease Research, Division of Hepato-Biliary-Pancreatic Surgery, Department of Surgery, The Second Xiangya Hospital, Central South University, 139 Renminzhong Road, Changsha, 410011, People's Republic of China. xuxundi@csu.edu.cn.
Central South University · CNSecond Xiangya Hospital of Central South University · CNBeth Israel Deaconess Medical Center · USKyushu University · JPOsaka University · JP

Funding

Hunan Provincial Key Research and Development Program 2019SK2242National Natural Science Foundation of China 81670111
6 · The paper itself

Abstract

backgroundLiver fibrosis represent a major global health care burden. Data emerging from recent advances suggest TRPM8, a member of the transient receptor potential (TRP) family of ion channels, plays an essential role in various chronic inflammatory diseases. However, its role in liver fibrosis remains unknown. Herein, we assessed the potential effect of TRPM8 in liver fibrosis.

methodsThe effect of TRPM8 was evaluated using specimens obtained from classic murine models of liver fibrosis, namely wild-type (WT) and TRPM8

resultsClinicopathological analysis showed that TRPM8 expression was upregulated in tissue samples from cirrhosis patients and fibrotic mice. TRPM8 deficiency not only attenuated inflammation and fibrosis progression in mice but also helped to alleviate symptoms of cholangiopathies. Moreover, reduction in S100A9 and increase in HNF4α expressions were observed in liver of CCl

conclusionsThese findings suggest TRPM8 deficiency may exert protective effects against inflammation, cholangiopathies, and fibrosis through S100A9-HNF4α signaling. M8-B might be a promising therapeutic candidate for liver fibrosis.

Indexed as

ECMHNF4αInflammationLiver fibrosisS100A9TRPM8

Identifiers

PMID35525986
PMCPMC9080211
OpenAlexW4229019507

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.