Li B, Ming RX, Liu YM, Zhang TJ. CD146-positive mesenchymal stromal cells: A promising subtype for enhanced acute respiratory distress syndrome therapy. World J Stem Cells 2025; 17(11): 114031 [DOI: 10.4252/wjsc.v17.i11.114031]
Corresponding Author of This Article
Bin Li, PhD, Assistant Professor, Institute of Comparative Medicine, Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, No. 88 Daxue South Road, Yangzhou 225009, Jiangsu Province, China. 008480@yzu.edu.cn
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Biology
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Letter to the Editor
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This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Nov 26, 2025 (publication date) through Nov 26, 2025
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World Journal of Stem Cells
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1948-0210
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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA
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Li B, Ming RX, Liu YM, Zhang TJ. CD146-positive mesenchymal stromal cells: A promising subtype for enhanced acute respiratory distress syndrome therapy. World J Stem Cells 2025; 17(11): 114031 [DOI: 10.4252/wjsc.v17.i11.114031]
World J Stem Cells. Nov 26, 2025; 17(11): 114031 Published online Nov 26, 2025. doi: 10.4252/wjsc.v17.i11.114031
CD146-positive mesenchymal stromal cells: A promising subtype for enhanced acute respiratory distress syndrome therapy
Bin Li, Rui-Xi Ming, Yu-Meng Liu, Tang-Jie Zhang
Bin Li, Rui-Xi Ming, Yu-Meng Liu, Tang-Jie Zhang, Institute of Comparative Medicine, Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, Jiangsu Province, China
Bin Li, Center for Integrative Physiology and Molecular Medicine, University of Saarland, Homburg 66424, Saarland, Germany
Yu-Meng Liu, College of Biological Sciences and Technology, Yangzhou University, Yangzhou 225009, Jiangsu Province, China
Co-corresponding authors: Bin Li and Tang-Jie Zhang.
Author contributions: Li B contributed to the manuscript writing, conceptualization, and project administration; Li B, Ming RX, Liu YM, and Zhang TJ contributed to the manuscript reviewing and editing, and participated in the formal analysis. Li B and Zhang TJ designed the study and supervised the project; they contributed equally to this manuscript and are co-corresponding authors. All authors participated in manuscript discussing.
Supported by the Basic Research Program of Jiangsu Province (2024), No. BK20240907; the “Lv Yang Jin Feng” Outstanding Doctor of Yangzhou, No. YZLYJFJH2023YXBS169; and the Top-Level Talents Support Program of Yangzhou University.
Conflict-of-interest statement: The authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Bin Li, PhD, Assistant Professor, Institute of Comparative Medicine, Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, No. 88 Daxue South Road, Yangzhou 225009, Jiangsu Province, China. 008480@yzu.edu.cn
Received: September 10, 2025 Revised: October 9, 2025 Accepted: October 28, 2025 Published online: November 26, 2025 Processing time: 77 Days and 18 Hours
Abstract
Acute respiratory distress syndrome (ARDS) remains without effective targeted reparative therapies and continues to carry a high mortality rate. Here, we comment on a recent study by Zhang et al, who identify a CD146+ subpopulation of mesenchymal stromal cells (MSCs) with superior reparative function in lipopolysaccharide-induced ARDS in mice. Compared with CD146- MSCs, CD146+ MSCs secreted higher levels of reparative paracrine mediators, including hepatocyte growth factor, vascular endothelial growth factor, prostaglandin E2 (PGE2), and angiopoietin 1, better preserved endothelial junctional proteins (VE-cadherin, zonula occludens-1), and more effectively modulated T cell and macrophage phenotypes. Mechanistic studies link these effects to a nuclear factor kappa B (NF-κB)/cyclooxygenase-2/PGE2 signaling axis, as pharmacologic blockade of NF-κB (caffeic acid phenethyl ester) abrogated the benefits. We place these results in the context of MSC heterogeneity research, highlight strengths (mechanistic depth, in vivo validation) and limitations (single animal model, reliance on cell lines rather than primary human cells), and propose next steps: Testing efficacy across diverse ARDS etiologies (viral, aspiration), validating effects in primary human alveolar and endothelial cells, delineating the CD146/NF-κB cascade, developing potency biomarkers (e.g., PGE2), and performing rigorous safety profiling. Strategies to enrich or prime MSCs for CD146-associated NF-κB/cyclooxygenase-2/PGE2 program activity may provide a practical route to higher potency.
Core Tip: This article presents evidence that CD146+ mesenchymal stromal cells define a high-potency subpopulation for acute respiratory distress syndrome therapy by engaging a nuclear factor kappa B → cyclooxygenase-2 paracrine signaling program. Enriching or priming mesenchymal stromal cells for CD146 expression and nuclear factor kappa B/cyclooxygenase-2 activity may yield practical potency biomarkers and enable more consistent, mechanism-driven cell therapies that more effectively restore alveolar-capillary barrier integrity.
