Evidence map›Paper›PMID 42218444›Full record

ArticleRespiratory research2026

The β-hydroxybutyrylation of Zyxin ameliorates pulmonary fibrosis by inhibiting lung fibroblast activation through the PI3K/AKT pathway.

Li Qiu, Haoying Huang, Sen Li, Haixia Chen, Xiaohui Wang

Abstract read
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In one paragraph

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

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1 · What the graph read from it

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Li QiuGuangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, 510623, China.
Haoying HuangGuangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, 510623, China.
Sen LiGuangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, 510623, China.
Haixia ChenGuangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, 510623, China.
Xiaohui WangGuangzhou Women and Children's Medical Center, State Key Laboratory of Respiratory Disease, Guangdong Basic Research Center of Excellence for Respiratory Medicine, Guangzhou Medical University, Guangzhou, 510623, China. xiaohuiwang2021621818@gzhmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a lethal interstitial lung disease with poorly understood pathogenesis. Here, we identify reduced lysine β-hydroxybutyrylation (Kbhb) of the focal adhesion protein Zyxin in bleomycin (BLM)-induced pulmonary fibrosis in mice. In a BLM-induced mouse model, we observe a significant reduction in lung tissue Kbhb levels, while β-hydroxybutyrate (β-OHB) supplementation restores Kbhb modification, there by mitigating fibrosis. Transcriptome profiling suggests that β-OHB exerts anti-fibrotic effects by modulating the PI3K/AKT pathway. Proteomic analysis further reveals a decrease in Kbhb modification at the K263 site of Zyxin in IPF mice. In vivo experiments demonstrate that Zyxin knockout or β-OHB treatment markedly alleviates fibrotic pathology and reduces collagen deposition as well as mouse mortality. This study is the first to elucidate the mechanism by which Zyxin Kbhb modification suppresses pulmonary fibrosis via the PI3K/AKT pathway, offering a novel metabolic modification-based therapeutic strategy for IPF.

Indexed as

3-Hydroxybutyric AcidFibroblastsLungPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPulmonary FibrosisZyxinAnimalsBleomycinMaleMiceMice, Inbred C57BLMice, KnockoutSignal Transduction3-Hydroxybutyric AcidBleomycinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktZyxinFibroblast activationPI3K/AKT pathwayPulmonary fibrosisZyxinβ-hydroxybutyrate supplementationβ-hydroxybutyrylation

Identifiers

PMID42218444
PMCPMC13479915

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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.