<scp>CXCR7</scp> Facilitates the Migration and Proliferation of <scp>UCMSCs</scp> via β‐Catenin/ <scp>TCF4</scp> / <scp>MDM2</scp> Signal Regulating Notch1 Ubiquitination to Ameliorate Pulmonary Fibrosis in <scp>ARDS</scp>

Umbilical cord mesenchymal stem cells (UCMSCs) hold therapeutic potential for acute respiratory distress syndrome (ARDS), but the role of atypical CXC chemokine receptor 7 (CXCR7) in their homing and reparative effects remains unclear. Using a lipopolysaccharide (LPS)-induced ARDS mouse model, we demonstrated that CXCR7 overexpression enhances UCMSC proliferation, migration, and lung repair. Mechanistically, CXCR7 activates the Wnt/β-catenin pathway to upregulate murine double minute (MDM2) transcription, which subsequently ubiquitinates and degrades Notch1, revealing a novel Wnt-Notch crosstalk. These findings highlight CXCR7 as a therapeutic target for ARDS and provide insights into UCMSC-based regenerative strategies.

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Publication Details

Journal
The FASEB Journal
Published
2025-10-01
DOI
https://doi.org/10.1096/fj.202500609rr
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Type
article
Field-Weighted Citation Impact
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article

CXCR7 Facilitates the Migration and Proliferation of UCMSCs via β‐Catenin/ TCF4 / MDM2 Signal Regulating Notch1 Ubiquitination to Ameliorate Pulmonary Fibrosis in ARDS

Jiahui Jin, Lixin Xie, David Y.B. Deng, Kun Xiao et al.
The FASEB Journal
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
article

CXCR7 Facilitates the Migration and Proliferation of UCMSCs via β‐Catenin/ TCF4 / MDM2 Signal Regulating Notch1 Ubiquitination to Ameliorate Pulmonary Fibrosis in ARDS

Jiahui Jin, Lixin Xie, David Y.B. Deng, Kun Xiao, Zhi Rong Qian, Yan Cao, Yuwei Yang, Shuning Zhang
article en

Abstract

Umbilical cord mesenchymal stem cells (UCMSCs) hold therapeutic potential for acute respiratory distress syndrome (ARDS), but the role of atypical CXC chemokine receptor 7 (CXCR7) in their homing and reparative effects remains unclear. Using a lipopolysaccharide (LPS)-induced ARDS mouse model, we demonstrated that CXCR7 overexpression enhances UCMSC proliferation, migration, and lung repair. Mechanistically, CXCR7 activates the Wnt/β-catenin pathway to upregulate murine double minute (MDM2) transcription, which subsequently ubiquitinates and degrades Notch1, revealing a novel Wnt-Notch crosstalk. These findings highlight CXCR7 as a therapeutic target for ARDS and provide insights into UCMSC-based regenerative strategies.

The FASEB JournalVol. 39(19)
Fujian Medical University (CN), Sun Yat-sen University (CN), Capital Medical University (CN), Chinese PLA General Hospital (CN), The Seventh Affiliated Hospital of Sun Yat-sen University (CN), PLA 306 Hospital (CN), Beijing Xuanwu Traditional Chinese Medicine Hospital (CN), PLA Academy of Military Science (CN), Union Hospital (CN)
Openalex Percentile: Top 60%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
DOISourceOpenAlex
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<scp>CXCR7</scp> Facilitates the Migration and Proliferation of <scp>UCMSCs</scp> via β‐Catenin/ <scp>TCF4</scp> / <scp>MDM2</scp> Signal Regulating Notch1 Ubiquitination to Ameliorate Pulmonary Fibrosis in <scp>ARDS</scp> — Jiahui Jin, Lixin Xie, et al. · The FASEB Journal (2025) | TGRS Research Map | TGRS