Evidence map›Paper›PMID 37484431›Full record

ReviewHeliyon2023

Exploring the potential of treating chronic liver disease targeting the PI3K/Akt pathway and polarization mechanism of macrophages.

Yaqian Yang, Xiaotao Jia, Mengyang Qu, Xinmao Yang, Yan Fang, Xiaoping Ying, Meiqian Zhang, Jing Wei, Yanfang Pan

Open access · goldAbstract readReview
In one paragraph

Review in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

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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.

Yaqian YangDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Xiaotao JiaDepartment of Neurology, The Affifiliated Xi'an Central Hospital of Xi'an Jiaotong University College of Medicine, Xi'an, Shaanxi 710003, PR China.
Mengyang QuDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Xinmao YangDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Yan FangDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Xiaoping YingDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Meiqian ZhangDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Jing WeiDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Yanfang PanDepartment of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
Shaanxi University of Chinese Medicine · CNXian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic liver disease is a significant public health issue that can lead to considerable morbidity and mortality, imposing an enormous burden on healthcare resources. Understanding the mechanisms underlying chronic liver disease pathogenesis and developing effective treatment strategies are urgently needed. In this regard, the activation of liver resident macrophages, namely Kupffer cells, plays a vital role in liver inflammation and fibrosis. Macrophages display remarkable plasticity and can polarize into different phenotypes according to diverse microenvironmental stimuli. The polarization of macrophages into M1 pro-inflammatory or M2 anti-inflammatory phenotypes is regulated by complex signaling pathways such as the PI3K/Akt pathway. This review focuses on investigating the potential of using plant chemicals targeting the PI3K/Akt pathway for treating chronic liver disease while elucidating the polarization mechanism of macrophages under different microenvironments. Studies have demonstrated that inhibiting M1-type macrophage polarization or promoting M2-type polarization can effectively combat chronic liver diseases such as alcoholic liver disease, non-alcoholic fatty liver disease, and liver fibrosis. The PI3K/Akt pathway acts as a pivotal modulator of macrophage survival, migration, proliferation, and their responses to metabolism and inflammatory signals. Activating the PI3K/Akt pathway induces anti-inflammatory cytokine expression, resulting in the promotion of M2-like phenotype to facilitate tissue repair and resolution of inflammation. Conversely, inhibiting PI3K/Akt signaling could enhance the M1-like phenotype, which exacerbates liver damage. Targeting the PI3K/Akt pathway has tremendous potential as a therapeutic strategy for regulating macrophage polarization and activity to treat chronic liver diseases with plant chemicals, providing new avenues for liver disease treatment.

Indexed as

Chronic liver diseaseMacrophage polarizationPI3K/Akt signaling pathwayTherapeutic strategy

Identifiers

PMID37484431
PMCPMC10361319
OpenAlexW4380200767

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.