Evidence map›Paper›PMID 40072374›Full record

ReviewAging and disease2025

Decoding Microglial Polarization and Metabolic Reprogramming in Neurodegenerative Diseases: Implications for Disease Progression and Therapy.

Ran Gao, Ya Gao, Wenting Su, Renxi Wang

Abstract readReview
In one paragraph

Review in Aging and disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

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  16. Microglial Feimin Alleviates Cognitive Impairment in High-Fat Diet-Fed Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  17. Proteomic Identification of ALDOA as a Pathogenic TDP-43 Interaction Partner in ALS.Degenerative neurological and neuromuscular disease · 2025
    Article
  18. 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

4 authors.

Ran GaoBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing 100069, China.
Ya GaoDepartment of Cardiology, The Second Medical Centre, Chinese PLA General Hospital, Beijing, 100853, China.
Wenting SuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing 100069, China.
Renxi WangBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, Beijing 100069, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the resident macrophages of the brain, microglia are crucial immune cells specific to the central nervous system (CNS). They constantly surveil their surroundings and trigger immunological reactions, playing a key role in various neurodegenerative diseases (ND). As illnesses progress, microglia exhibit multiple phenotypes. Traditionally, microglia have been classified into two main phenotypes upon activation: the pro-inflammatory M1 polarization and the anti-inflammatory M2 polarization. However, this classification is now considered overly simplistic, as it is unable to fully convey the intricacy and diversity of the inflammatory response. Immune regulatory factors, such as chemokines secreted by microglia, are essential for modulating brain development, maintaining the neural milieu, and orchestrating responses to injury, along with the subsequent repair processes. However, in recent years, the significance of metabolic reprogramming in both physiological microglial activity and ND has also become increasingly recognized. Upon activation-triggered by brain injury, infection, or ND-microglia typically modify their metabolic processes by transitioning from oxidative phosphorylation (OXPHOS) phosphorylation to glycolysis. This shift facilitates rapid energy production but may also enhance pro-inflammatory responses. This review seeks to summarize metabolic reprogramming and polarization in the function of microglia and their involvement in ND.

Indexed as

MicrogliaNeurodegenerative DiseasesAnimalsBrainDisease ProgressionHumansMetabolic Reprogramming

Identifiers

PMID40072374
PMCPMC12730189

What OpenQuestion holds

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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.