Evidence map›Paper›PMID 38992119›Full record

ArticleActa pharmacologica Sinica2024

FXR activation remodels hepatic and intestinal transcriptional landscapes in metabolic dysfunction-associated steatohepatitis.

Ying-Quan Wen, Zi-Yuan Zou, Guan-Guan Zhao, Meng-Jiao Zhang, Yong-Xin Zhang, Gai-Hong Wang, Jing-Jing Shi, Yuan-Yang Wang, Ye-Yu Song, Hui-Xia Wang and 7 more

Abstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
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  11. Targeting Metabolism: Innovative Therapies for MASLD Unveiled.International journal of molecular sciences · 2025
    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

17 authors.

Ying-Quan Wen *School of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China.
Zi-Yuan Zou *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Guan-Guan Zhao *State Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Meng-Jiao ZhangSchool of Chinese Materia Medica, Nanjing University of Chinese Medicine, Nanjing, 210029, China.
Yong-Xin ZhangState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Gai-Hong WangCascade Pharmaceuticals, Inc, Shanghai, 201321, China.
Jing-Jing ShiCascade Pharmaceuticals, Inc, Shanghai, 201321, China.
Yuan-Yang WangState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Ye-Yu SongState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China.
Hui-Xia WangCascade Pharmaceuticals, Inc, Shanghai, 201321, China.
Ru-Ye ChenCascade Pharmaceuticals, Inc, Shanghai, 201321, China.
Dong-Xuan ZhengCascade Pharmaceuticals, Inc, Shanghai, 201321, China.
Xiao-Qun DuanIndustrial Technology Research Institute of Pharmacy, Guilin Medical University, Guilin, 541199, China.
Ya-Meng LiuState Key Laboratory of Drug Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, 201203, China. yameng_liu@simm.ac.cn.ORCID http://orcid.org/0000-0003-2970-2308
Frank J GonzalezLaboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Jian-Gao FanDepartment of Gastroenterology, Center for Fatty Liver, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Key Lab of Pediatric Gastroenterology and Nutrition, Shanghai, 200092, China. fanjiangao@xinhuamed.com.cn.ORCID http://orcid.org/0000-0002-8618-6402
Cen XieSchool of Pharmacy, Jiangxi Medical College, Nanchang University, Nanchang, 330006, China. xiecen@simm.ac.cn.ORCID http://orcid.org/0000-0002-4574-8456

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The escalating obesity epidemic and aging population have propelled metabolic dysfunction-associated steatohepatitis (MASH) to the forefront of public health concerns. The activation of FXR shows promise to combat MASH and its detrimental consequences. However, the specific alterations within the MASH-related transcriptional network remain elusive, hindering the development of more precise and effective therapeutic strategies. Through a comprehensive analysis of liver RNA-seq data from human and mouse MASH samples, we identified central perturbations within the MASH-associated transcriptional network, including disrupted cellular metabolism and mitochondrial function, decreased tissue repair capability, and increased inflammation and fibrosis. By employing integrated transcriptome profiling of diverse FXR agonists-treated mice, FXR liver-specific knockout mice, and open-source human datasets, we determined that hepatic FXR activation effectively ameliorated MASH by reversing the dysregulated metabolic and inflammatory networks implicated in MASH pathogenesis. This mitigation encompassed resolving fibrosis and reducing immune infiltration. By understanding the core regulatory network of FXR, which is directly correlated with disease severity and treatment response, we identified approximately one-third of the patients who could potentially benefit from FXR agonist therapy. A similar analysis involving intestinal RNA-seq data from FXR agonists-treated mice and FXR intestine-specific knockout mice revealed that intestinal FXR activation attenuates intestinal inflammation, and has promise in attenuating hepatic inflammation and fibrosis. Collectively, our study uncovers the intricate pathophysiological features of MASH at a transcriptional level and highlights the complex interplay between FXR activation and both MASH progression and regression. These findings contribute to precise drug development, utilization, and efficacy evaluation, ultimately aiming to improve patient outcomes.

Indexed as

LiverMice, KnockoutReceptors, Cytoplasmic and NuclearAnimalsFatty LiverHumansIntestinal MucosaIntestinesMaleMiceMice, Inbred C57BLReceptor, Farnesoid X-ActivatedTranscriptomeReceptor, Farnesoid X-ActivatedReceptors, Cytoplasmic and NuclearagonistFXRgut-liver axisMASLD/MASHtranscriptome

Identifiers

PMID38992119
PMCPMC11489735

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.