Evidence map›Paper›PMID 39951182›Full record

ArticleNeuroscience bulletin2025

Fto-dependent Vdac3 m6A Modification Regulates Neuronal Ferroptosis Induced by the Post-ICH Mass Effect and Transferrin.

Zhongmou Xu, Haiying Li, Xiang Li, Jinxin Lu, Chang Cao, Lu Peng, Lianxin Li, John Zhang, Gang Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

9 authors.

Zhongmou Xu *Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Haiying Li *Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Xiang Li *Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Jinxin LuDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China. ljx54257@163.com.ORCID http://orcid.org/0000-0002-0929-0804
Chang CaoDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Lu PengDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
Lianxin LiDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China.
John ZhangDepartments of Neurosurgery, Anesthesiology, Physiology and Pharmacology, Pathology and Human Anatomy, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
Gang ChenDepartment of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Soochow University, Suzhou, 215006, China. nju_neurosurgery@163.com.ORCID http://orcid.org/0000-0002-0758-1907

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the hyperacute phase of intracerebral hemorrhage (ICH), the mass effect and blood components mechanically lead to brain damage and neurotoxicity. Our findings revealed that the mass effect and transferrin precipitate neuronal oxidative stress and iron uptake, culminating in ferroptosis in neurons. M6A (N6-methyladenosine) modification, the most prevalent mRNA modification, plays a critical role in various cell death pathways. The Fto (fat mass and obesity-associated protein) demethylase has been implicated in numerous signaling pathways of neurological diseases by modulating m6A mRNA levels. Regulation of Fto protein levels in neurons effectively mitigated mass effect-induced neuronal ferroptosis. Applying nanopore direct RNA sequencing, we identified voltage-dependent anion channel 3 (Vdac3) as a potential target associated with ferroptosis. Fto influenced neuronal ferroptosis by regulating the m6A methylation of Vdac3 mRNA. These findings elucidate the intricate interplay between Fto, Vdac3, m6A methylation, and ferroptosis in neurons during the hyperacute phase post-ICH and suggest novel therapeutic strategies for ICH.

Indexed as

AdenosineAlpha-Ketoglutarate-Dependent Dioxygenase FTOFerroptosisNeuronsTransferrinAnimalsMaleMethylationMiceMice, Inbred C57BLOxidative StressRNA, MessengerAdenosineAlpha-Ketoglutarate-Dependent Dioxygenase FTOFTO protein, mouseN-methyladenosineRNA, MessengerTransferrinFerroptosisIntracerebral hemorrhageM6A methylationMass effectTransferrinVdac3

Identifiers

PMID39951182
PMCPMC12158900

What Socratic holds

Textmetadata
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.