Evidence map›Paper›PMID 40308001›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Neuronal C/EBPβ Shortens the Lifespan via Inactivating NAMPT.

Bowei Li, Zhongyun Xie, Mengmeng Wang, Shuke Nie, Zhengjiang Qian, Xin Meng, Xia Liu, Seong Su Kang, Keqiang Ye

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Neuronal C/EBPβ Shortens the Lifespan via Inactivating NAMPT.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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.

Bowei LiBrain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.ORCID https://orcid.org/0000-0002-5624-9361
Zhongyun XieBrain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.
Mengmeng WangBrain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.
Shuke NieDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China.
Zhengjiang QianBrain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.
Xin MengBrain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.
Xia LiuDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Seong Su KangDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Keqiang YeBrain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China.ORCID https://orcid.org/0000-0002-7657-8154

Funding

ApoE4 and C/EBP: Mutually Regulate Each Other in Alzheimer's DiseaseR01AG065177 · NIA · EMORY UNIVERSITY · PI BENIAN, GUY MARTIN · 2020 to 2024
$2.3M
Guangdong Basic and Applied Basic Research Foundation 2023A1515030296National Natural Science Foundation of China 32330040National Natural Science Foundation of China 82350710222NIA NIH HHS R01 AG065177Shenzhen Government Basic Research Program JCYJ20220531100802005Shenzhen Science and Technology Program KQTD20221101093608028
6 · The paper itself

Abstract

The brain plays a central role in aging and longevity in diverse model organisms. Morphological and functional alteration in the aging brain elicits age-associated neuronal dysfunctions. However, the primary mechanism deteriorating the brain functions to regulate the aging process remains incompletely understood. Here, it is shown that neuronal CCAAT/enhancer binding protein β (C/EBPβ) escalation during aging dictates the frailty and lifespan via inactivating nicotinamide phosphoribosyltransferase (NAMPT). Upregulated C/EBPβ drives neuronal senescence and neuronal loss, associated with NAMPT fragmentation by active asparagine endopeptidase (AEP), leading to nicotinamide adenine dinucleotide (NAD

Indexed as

AgingCCAAT-Enhancer-Binding Protein-betaCytokinesLongevityNeuronsNicotinamide PhosphoribosyltransferaseAnimalsCaenorhabditis elegansHumansMiceMice, TransgenicNADCCAAT-Enhancer-Binding Protein-betaCytokinesNADNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, mouseasparagine endopeptidase (AEP)brain agingCCAAT/enhancer binding protein β (C/EBPβ)nicotinamide adenine dinucleotide (NAD+)nicotinamide phosphoribosyltransferase (NAMPT)

Identifiers

PMID40308001
PMCPMC12140299

What OpenQuestion holds

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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.