ESRP1 drives epithelial-mesenchymal transition by activating EPAC-RAP1A signaling axis.

Ruixin Qi, Jiaqi Wang, Guocang Cheng, Tingting Zhao, Zhengyu Hu, Jialin Yu, Yuanyuan Jia, Juan Chen

Abstract read

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Article in Frontiers in medicine, 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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5 · Who and what money

Authors and funding

8 authors.

Ruixin QiNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Jiaqi WangNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Guocang ChengDepartment of Respiratory and Critical Care Medicine, Qingyang People's Hospital, Qingyang, Gansu, China.

Tingting ZhaoNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Zhengyu HuNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Jialin YuNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Yuanyuan JiaNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Juan ChenNingxia Key Laboratory of Clinical and Pathogenic Microorganisms, Institute of Medical Science, General Hospital of Ningxia Medical University, Yinchuan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Idiopathic pulmonary fibrosis (IPF) is a fatal lung disease characterized by epithelial-mesenchymal transition (EMT) as a key pathological feature. The molecular mechanism of EMT is not fully understood. Hence, the current study aimed to investigate the pathogenesis of EMT, which focus on the function of Epithelial Splicing Regulatory Protein 1 (ESRP1) in regulating EMT. Methods: The present study utilized bleomycin (BLM) to establish mouse models of IPF. Then, single-cell RNA sequencing (scRNA-seq) of entire lung tissue was employed to delineate transcriptional alterations in epithelial cells and to nominate prospective regulators of EMT. The target gene was subsequently validated Results: ScRNA-seq revealed marked up-regulation of the ESRP1 in alveolar epithelial cells compared with PBS-treated controls. Subsequent mechanistic interrogation in primary and MLE-12 alveolar epithelial cells demonstrated that knockdown of ESRP1 suppressed, whereas its overexpression potentiated, the expression of Epac, Rap1a, and N-cad which were key effectors of EMT. Importantly, Co-IP (Co-Immunoprecipitation) showed that there was interaction between ESRP1, Epac, and Rap1a. Silencing of either Epac or Rap1a did not reciprocally alter ESRP1 expression, confirming an upstream regulatory hierarchy. Conclusion: Our findings demonstrate that ESRP1 upregulation in alveolar epithelial cells drives IPF progression by promoting EMT via the Epac-Rap1a axis.

Indexed as

Epac-Rap1a signalingepithelialepithelial-mesenchymal transition (EMT)epithelial splicing regulatory protein 1 (ESRP1)idiopathic pulmonary fibrosissingle-cell RNA sequencing (scRNA-seq)

Identifiers

PMID41728622

DOI10.3389/fmed.2026.1734619

PMCPMC12920467

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