Evidence map›Paper›PMID 41412037›Full record

ArticleRedox biology2026

Acetylation of fatty acid synthase regulates microglial lipid droplets accumulation and pro-inflammatory activity following traumatic brain injury.

Fengchen Zhang, Tao Lv, Tianqi Xu, Jie Li, Jie Lian, Siyu Lin, Qin Hu, Yichao Jin, Feng Jia, Xiaohua Zhang

Abstract read
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

10 authors.

Fengchen ZhangDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. Electronic address: zhangfengchen@renji.com.
Tao LvDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. Electronic address: lvtao512@aliyun.com.
Tianqi XuDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Jie LiDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Jie LianDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Siyu LinDepartment of Endocrinology and Metabolism, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Qin HuDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Yichao JinDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. Electronic address: jinyichao@renji.com.
Feng JiaDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China; Department of Neurosurgery, Nantong First People's Hospital, Affiliated Hospital 2 of Nantong University, Nantong, Jiangsu, 226001, China. Electronic address: projiafeng@163.com.
Xiaohua ZhangDepartment of Neurosurgery, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. Electronic address: zxh1969@aliyun.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lipid droplet accumulation in microglia has been implicated in inflammatory functions associated with aging and demyelinating diseases. However, the molecular mechanisms driving lipid droplet formation under pathological conditions remain unrevealed. It is demonstrated herein that the acetylation of fatty acid synthase (FASN) plays a key regulatory role in the accumulation of lipid droplets in microglia following traumatic brain injury (TBI). Through mass spectrometry analysis, we identified hyperacetylation at lysine K673 of FASN as a critical driver of lipid droplet formation in microglia. Notably, this acetylation event not only promotes lipid droplet accumulation but also enhances pro-inflammatory cytokine production and phagocytic activity in microglia. Additionally, we found that HDAC3 may be the enzyme responsible for deacetylation of FASN K673. Importantly, observation of a mouse model carrying the FASN K673R mutation revealed a reduction in microglial lipid droplet accumulation and neuroinflammatory responses following TBI relative to wild-type mice. Thus, FASN acetylation is a pivotal regulator of post-TBI microglial lipid droplet formation and neuroinflammation. This positions the targeting of deacetylation pathways as a novel therapeutic strategy for TBI.

Indexed as

Brain Injuries, TraumaticFatty Acid Synthase, Type ILipid DropletsMicrogliaAcetylationAnimalsCytokinesDisease Models, AnimalHumansInflammationMaleMiceCytokinesFasn protein, mouseFatty Acid Synthase, Type IAcetylationFatty acid synthaseMicrogliaNeuroinflammationTraumatic brain injury

Identifiers

PMID41412037
PMCPMC12808841

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.