Evidence map›Paper›PMID 38250155›Full record

ArticleInternational journal of biological sciences2024

Inactivation of MST1/2 Controls Macrophage Polarization to Affect Macrophage-Related Disease via YAP and Non-YAP Mechanisms.

Yina An, Shuyu Tan, Pu Zhang, Jingjing Yang, Kezhi Wang, Ruicheng Zheng, Lu Qiao, Yang Wang, Yanjun Dong

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
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  10. Review
  11. YAP activation in liver macrophages via depletion of MST1/MST2 enhances liver inflammation and fibrosis in MASLD.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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

9 authors at 2 institutions in 1 country.

Yina AnDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Shuyu TanDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Pu ZhangDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Jingjing YangDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Kezhi WangDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Ruicheng ZhengBeijing Key Laboratory of Detection Technology for Animal-Derived Food Safety, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Lu QiaoBeijing Key Laboratory of Detection Technology for Animal-Derived Food Safety, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Yang WangBeijing Key Laboratory of Detection Technology for Animal-Derived Food Safety, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
Yanjun DongDepartment of Basic Veterinary Medicine, College of Veterinary Medicine, China Agricultural University; Beijing, 100193, China.
China Agricultural University · CNBeijing University of Agriculture · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage polarization is a critical process that regulates in inflammation, pathogen defense, and tissue repair. Here we demonstrate that MST1/2, a core kinase of Hippo pathway and a recently identified regulator of inflammation, plays a significant role in promoting M2 polarization. We provide evidence that inhibition of MST1/2, achieved through either gene-knockout or pharmacological treatment, leads to increased M1 polarization in a YAP-dependent manner, resulting in the development of M1-associated inflammatory disorders. Moreover, MST1/2 inhibition also leads to a substantial reduction in M2 polarization, but this occurs through the STAT6 and MEK/ERK signaling. The STAT6 is independent of YAP, but MEK/ERK is dependent of YAP. Consistent with these observations, both MST1/2-conditional knockout mice and wild-type mice treated with XMU-MP-1, a chemical inhibitor of MST1/2, exhibited reduced M2-related renal fibrosis, while simultaneously displaying enhanced LPS-mediated inflammation and improved clearance of MCR3-modified gram-negative bacteria. These findings uncover a novel role of MST1/2 in regulating macrophage polarization and establish it as a potential therapeutic target for the treatment of macrophage-related fibrotic diseases.

Indexed as

InflammationMacrophage ActivationProtein Serine-Threonine KinasesAnimalsGene Knockout TechniquesHippo KinasesMacrophagesMiceMice, KnockoutMitogen-Activated Protein Kinase KinasesSerine-Threonine Kinase 3Hippo KinasesMitogen-Activated Protein Kinase KinasesProtein Serine-Threonine KinasesSerine-Threonine Kinase 3Stk3 protein, mouseStk4 protein, mousebacterial infectioninflammatory diseasemacrophage polarizationMST1/2UUO

Identifiers

PMID38250155
PMCPMC10797691
OpenAlexW4391036554

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.