Evidence map›Paper›PMID 41535860›Full record

ArticleJournal of nanobiotechnology2026

Extracellular vesicles from alveolar macrophages promotes pulmonary fibrosis through suppression of lung alveolar regeneration.

Jiali Min, Yu Zhang, Jiahui Yang, Suosi Liu, Qianrong Wang, Xiangning Tang, Fangfang Yuan, Zhenkun Xia, Xia Li, Hong Peng and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 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

13 authors.

Jiali Min *National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Yu Zhang *National Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Jiahui YangNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Suosi LiuNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Qianrong WangNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Xiangning TangNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Fangfang YuanDepartment of Critical Care Medicine, The 3rd Xiangya Hospital, Central South University, Changsha, China.
Zhenkun XiaDepartment of Chestsurgery, The Second Xiangya Hospital of Central South University, Changsha, China.
Xia LiNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China.
Hong PengDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital of Central South University, Changsha, China.
Zhiguang ZhouNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China. zhouzhiguang@csu.edu.cn.
Yang XiaoNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China. xiaoyang29@csu.edu.cn.
Shanshan LiuNational Clinical Research Center for Endocrine and Metabolic Diseases, Key Laboratory of Diabetes Immunology, Ministry of Education, and Department of Metabolism and Endocrinology, The Second Xiangya Hospital of Central South University, Changsha, China. lss0625@csu.edu.cn.

Funding

Beijing Natural Science Foundation 7222260Central South University Innovation-Driven Research Programme 2023CXQD026Hunan Provincial Health Commission Research Program A202302045948National Natural Science Foundation of China 81820108007 and 81800745National Natural Science Foundation of China 82322002 and 82273997National Science Foundation of Hunan Province for Excellent Young Scholars 2023JJ20084Natural Science Foundation of Hunan Province 2022JJ30820
6 · The paper itself

Abstract

Pulmonary fibrosis (PF) is a type of progressive interstitial lung disease characterized by varying degrees of lung interstitial fibrosis. Lung alveolar regeneration failure in PF is critical for mediating this incurable disease. Here, we report that chronic lung injury induces the release of extracellular vesicles (EVs) from alveolar macrophages (AMs) to promote PF development by inhibiting alveolar regeneration. Mechanistically, the acetylation of mixed lineage kinase domain-like protein (MLKL), which is mediated by the upregulation of acetylase lysine acetyltransferase 5 (KAT5) following chronic lung injury, enhances its capacity to facilitate endosomal trafficking and the production of EVs from AMs. Those EVs, which are taken up by type 2 alveolar epithelial cells (AEC2s), release miR-148a-3p to repress the endogenous β-catenin agonist Wnt10b and exert an inhibitory effect on AEC2 renewal. Disruption of the KAT5-MLKL interaction or pharmacological inhibition of miR-148a-3p expression restores the regenerative capacity of AEC2s, with potent therapeutic efficacy in PF. Our study suggests a potential therapeutic option for PF.

Indexed as

Extracellular VesiclesMacrophages, AlveolarPulmonary AlveoliPulmonary FibrosisRegenerationAlveolar Epithelial CellsAnimalsHumansLungMaleMiceMice, Inbred C57BLMicroRNAsMicroRNAsAlveolar macrophageExtracellular vesiclesLung regenerationProtein‒protein interactionPulmonary fibrosis

Identifiers

PMID41535860
PMCPMC12888306

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.