Evidence map›Paper›PMID 36529923›Full record

ReviewCurrent neuropharmacology2023

Metabolic Reprogramming of Microglia in Sepsis-Associated Encephalopathy: Insights from Neuroinflammation.

Shenjia Gao, Yi Jiang, Zhaoyuan Chen, Xiaoqiang Zhao, Jiahui Gu, Han Wu, Yun Liao, Hao Sun, Jun Wang, Wankun Chen

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
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  3. Metabolic Reprogramming of Microglia in Neuroinflammation and Depression.International journal of molecular sciences · 2026
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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

10 authors at 4 institutions in 1 country.

Shenjia GaoDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Yi JiangDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Zhaoyuan ChenDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Xiaoqiang ZhaoDepartment of Integrative Medicine and Neurobiology, School of Basic Medical Science, State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai, 200032, China.
Jiahui GuDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Han WuDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Yun LiaoShanghai Medical College of Fudan University, Shanghai, China.
Hao SunDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Jun WangDepartment of Integrative Medicine and Neurobiology, State Key Laboratory of Medical Neurobiology, School of Basic Medical Science, Fudan University, 200032 Shanghai, China.
Wankun ChenDepartment of Anesthesiology, Cancer Center, Zhongshan Hospital, Fudan University, 180# Feng-Lin Road, Shanghai, 200032, China.
Zhongshan Hospital · CNFudan University · CNShanghai Medical College of Fudan University · CNState Key Laboratory of Medical Neurobiology

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction caused by sepsis that manifests as a range of brain dysfunctions from delirium to coma. It is a relatively common complication of sepsis associated with poor patient prognosis and mortality. The pathogenesis of SAE involves neuroinflammatory responses, neurotransmitter dysfunction, blood-brain barrier (BBB) disruption, abnormal blood flow regulation, etc. Neuroinflammation caused by hyperactivation of microglia is considered to be a key factor in disease development, which can cause a series of chain reactions, including BBB disruption and oxidative stress. Metabolic reprogramming has been found to play a central role in microglial activation and executive functions. In this review, we describe the pivotal role of energy metabolism in microglial activation and functional execution and demonstrate that the regulation of microglial metabolic reprogramming might be crucial in the development of clinical therapeutics for neuroinflammatory diseases like SAE.

Indexed as

Brain DiseasesSepsisSepsis-Associated EncephalopathyBlood-Brain BarrierHumansMicrogliaNeuroinflammatory Diseasesmetabolic reprogrammingmicroglianeuroinflammationsepsisSepsis-associated encephalopathy

Identifiers

PMID36529923
PMCPMC10514522
OpenAlexW4311874429

What Socratic 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 Socratic graph.