Evidence map›Paper›PMID 41944369›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Activation of ERBB4 Pathway Inhibits Pathological Transdifferentiation of Lung Epithelial Progenitors into CD66c

Kaijun Lin, Xinran Deng, Haonan Wang, Yamei Jiang, Jian Sun, Hailin Ding, Ming Ye, Xiaoting Wang, Yu Wang, Li Yuan and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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

14 authors.

Kaijun LinState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0009-0008-1576-0025
Xinran DengState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Haonan WangState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Yamei JiangState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Jian SunDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Hailin DingDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Ming YeDepartment of Cardiothoracic Surgery, Children's Hospital, Fudan University, Shanghai, China.
Xiaoting WangState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Yu WangState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Li YuanDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Zhenju SongDepartment of Emergency Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
Xinhua LinState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Shenfei SunState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Ning JiangState Key Laboratory of Genetic and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0003-0664-6286

Funding

National Key Research and Development Program of China 2021YFC2501800National Key Research and Development Program of China 2022YFA0806200National Major Science and Technology Projects of China 2025ZD01902600National Natural Science Foundation of China 32192400National Natural Science Foundation of China 32300702National Natural Science Foundation of China 32350710191Science and Technology Projects in Guangzhou 2024D03J0014
6 · The paper itself

Abstract

Aberrant accumulation of basal cells in the distal lung is a hallmark of impaired epithelial regeneration and is closely associated with fibrotic remodeling; however, their cellular origins and the mechanisms governing their expansion remain unclear. Here, this study establishes human distal lung organoids (DLOs) as a physiologically relevant model to investigate epithelial repair. Single-cell transcriptomic and functional analyses identify a CD66c

Indexed as

Antigens, CDCell Adhesion MoleculesCell TransdifferentiationEpithelial CellsIdiopathic Pulmonary FibrosisLungLung InjuryReceptor, ErbB-4Stem CellsAnimalsHumansOrganoidsSignal TransductionAntigens, CDCell Adhesion MoleculesERBB4 protein, humanReceptor, ErbB-4CD66c+ basal cellsdistal lung organoidsepithelial plasticityERBB4 signalingidiopathic pulmonary fibrosis (IPF)

Identifiers

PMID41944369
PMCPMC13334660

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.