Evidence map›Paper›PMID 42089599›Full record

ArticleAnimal models and experimental medicine2026

SDPR-STK38 axis controls the proliferation-differentiation balance in alveolar type II cells.

Jie Wang, Xuepei Lei, Yiying Huang, Jiaming Tang, Guiying Shi, Hang Li, Lin Bai

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Animal models and experimental medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

7 authors.

Jie WangState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.ORCID https://orcid.org/0009-0008-2188-2520
Xuepei LeiState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.
Yiying HuangState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.
Jiaming TangState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.
Guiying ShiState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.
Hang LiState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.ORCID https://orcid.org/0000-0003-1815-4369
Lin BaiState Key Laboratory of Respiratory Health and Multimorbidity, Key Laboratory of Pathogen Infection Prevention and Control, Institute of Laboratory Animal Science, National Human Diseases Animal Model Resource Center, National Center of Technology Innovation for Animal Model, Chinese Academy of Medical Sciences and Peking Union Medical College, Ministry of Education, Beijing, China.ORCID https://orcid.org/0000-0002-0646-0812

Funding

CAMS Initiative for Innovative Medicine of China 2021-I2M-1-035Central Research Institute Fund of Chinese Academy of Medical Sciences 2023-PT330-01National Key Research and Development Program of China 2022YFA1105600
6 · The paper itself

Abstract

backgroundAlveolar type II (AT2) cells act as progenitors that sustain gas exchange and drive postinjury repair. Disruption of their proliferation-differentiation balance promotes pulmonary fibrosis and acute respiratory distress syndrome, but the core regulatory mechanisms are unclear. Serum deprivation response protein (SDPR, cavin-2), a caveolae-associated protein involved in proliferation and lipid metabolism, may modulate AT2 fate. This study investigated how the SDPR-STK38 axis regulates AT2 proliferation and differentiation and its impact on lung homeostasis and regeneration.

methodsSDPR knockout (SDPR

resultsSDPR deficiency disrupted alveolar architecture and impaired lung function, accompanied by excessive AT2 expansion and reduced differentiation into AT1 cells. Proteomic and biochemical analyses identified STK38 as a novel SDPR-binding protein. SDPR loss increased STK38 expression, enhanced GSK-3β/cyclin D1 signaling, and promoted AT2 proliferation, while simultaneously reducing Hes1 expression, impairing vacuole formation, and attenuating AT2 differentiation. In the LPS model, SDPR

conclusionsThe SDPR-STK38 axis coordinately controls the proliferation-differentiation balance of AT2 cells via GSK-3β/cyclin D1 and Notch-Hes1 signaling. SDPR deficiency drives aberrant AT2 expansion, blocks differentiation toward AT1 cells, and aggravates acute lung injury, highlighting this pathway as a potential therapeutic target for promoting alveolar regeneration.

Indexed as

AT2 cellGSK/3β–cyclin D1 pathwayNotch–Hes1 pathwaySDPRSTK38

Identifiers

PMID42089599
PMCPMC13394744

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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.