Evidence map›Paper›PMID 39387442›Full record

ReviewImmunity, inflammation and disease2024

Macrophages in the inflammatory response to endotoxic shock.

Xinjie Zhao, Mengjie Wang, Yanru Zhang, Yiyi Zhang, Haojie Tang, Hongyi Yue, Li Zhang, Dan Song

Abstract readReview
In one paragraph

Review in Immunity, inflammation and disease, 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. Article
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  9. Inflammatory factors collaboratively linkFrontiers in immunology · 2025
    Review
  10. Article
  11. Macrophages in the inflammatory response to endotoxic shock.Immunity, inflammation and disease · 2024
    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

8 authors.

Xinjie ZhaoKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
Mengjie WangKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
Yanru ZhangKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
Yiyi ZhangKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
Haojie TangKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
Hongyi YueKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.
Li ZhangAffiliated Hospital of Xizang Minzu University, Xianyang, Shaanxi, China.
Dan SongKey Laboratory for Molecular Genetic Mechanisms and Intervention Research on High Altitude Disease of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, Shaanxi, China.ORCID 0000-0002-7494-8078

Funding

Graduate Research Innovation and Practice Project of Xizang Minzu University Y2024004Graduate Research Innovation and Practice Project of Xizang Minzu University Y2024012National Natural Science Foundation of China 32160165Natural Science Foundation of Tibet Autonomous Region XZ202201ZR0065GYouth project of Xizang Minzu University 24MDQ06
6 · The paper itself

Abstract

backgroundEndotoxic shock, particularly prevalent in intensive care units, represents a significant medical challenge. Endotoxin, upon invading the host, triggers intricate interactions with the innate immune system, particularly macrophages. This activation leads to the production of inflammatory mediators such as tumor necrosis factor-alpha, interleukin-6, and interleukin-1-beta, as well as aberrant activation of the nuclear factor-kappa-B and mitogen-activated protein kinase signaling pathways.

objectiveThis review delves into the intricate inflammatory cascades underpinning endotoxic shock, with a particular focus on the pivotal role of macrophages. It aims to elucidate the clinical implications of these processes and offer insights into potential therapeutic strategies.

resultsMacrophages, central to immune regulation, manifest in two distinct subsets: M1 (classically activated subtype) macrophages and M2 (alternatively activated subtype) macrophages. The former exhibit an inflammatory phenotype, while the latter adopt an anti-inflammatory role. By modulating the inflammatory response in patients with endotoxic shock, these macrophages play a crucial role in restoring immune balance and facilitating recovery.

conclusionMacrophages undergo dynamic changes within the immune system, orchestrating essential processes for maintaining tissue homeostasis. A deeper comprehension of the mechanisms governing macrophage-mediated inflammation lays the groundwork for an anti-inflammatory, targeted approach to treating endotoxic shock. This understanding can significantly contribute to the development of more effective therapeutic interventions.

Indexed as

InflammationMacrophagesShock, SepticAnimalsHumansInflammation MediatorsMacrophage ActivationSignal TransductionInflammation Mediatorsendotoxic shockinflammationlipopolysaccharidemacrophagesNF‐κB/MAPK signaling pathway

Identifiers

PMID39387442
PMCPMC11465138

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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.