Evidence map›Paper›PMID 42463911›Full record

ArticleThe EMBO journal2026

Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.

Yihan Wang, Xiong Xiong, Runshuai Zhang, Long Xiao, Xinyu Ruan, Tianyi Ni, Zicheng Liu, Jie Chen, Shenlu Qin, Zhuo Du and 2 more

Abstract read
In one paragraph

Article in The EMBO journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Yihan WangSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.ORCID http://orcid.org/0009-0007-2080-2931
Xiong XiongSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.ORCID http://orcid.org/0009-0002-1243-1003
Runshuai ZhangSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Long XiaoInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Xinyu RuanSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Tianyi NiSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Zicheng LiuSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Jie ChenSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Shenlu QinSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Zhuo DuInstitute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.ORCID http://orcid.org/0000-0002-6322-4656
Yanxiao ZhangSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.ORCID http://orcid.org/0000-0001-9618-637X
Lianfeng WuSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China. wulianfeng@westlake.edu.cn.ORCID http://orcid.org/0000-0003-0237-2548

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Ann E. Rougvie · 2012 to 2026
$7.5M
MOST | National Natural Science Foundation of China (NSFC) 32071151MOST | National Natural Science Foundation of China (NSFC) 32271357MOST | NSFC | NSFC-Zhejiang Joint Fund | | Zhejiang Provincial Program for the Cultivation of High-Level Innovative Health Talents 2022XHSJJ005NIH HHS P40 OD010440
6 · The paper itself

Abstract

Proteostasis collapse, a hallmark of aging and neurodegeneration like Alzheimer's disease (AD), causes irreversible damage in late life. Whether late-life proteostasis capacity is developmentally programmed remains unclear, as mechanistic studies requiring lifelong tracking and molecular manipulation are challenging or impossible in long-lived species. Using C. elegans as a lifelong, genetically tractable AD model, we uncover a critical early-life window during which reducing TIP60/NuA4 acetyltransferase complex activity enduringly enhances proteostasis and extends lifespan. Mechanistically, NuA4 reduction depletes H4K16ac, triggering a compensatory, early-life-biased, XBP-1-mediated unfolded protein response (UPR

Indexed as

Caenorhabditis elegansCaenorhabditis elegans ProteinsHistone AcetyltransferasesLongevityProteostasisAlzheimer DiseaseAnimalsCarrier ProteinsEndoplasmic ReticulumLipid MetabolismOleic AcidProteotoxic StressUnfolded Protein ResponseCaenorhabditis elegans ProteinsCarrier ProteinsHistone AcetyltransferasesOleic AcidXBP-1 protein, C elegans

Identifiers

PMID42463911
PMCPMC13482575

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.