Zhang RQ, Chu WH, Bai JB, Lei YH, Zhou D. Selenoprotein P attenuates oxidative senescence and ferroptosis-associated lipid peroxidation in dental pulp stem cells through a FOXM1-dependent program. World J Stem Cells 2026; 18(6): 119118 [DOI: 10.4252/wjsc.119118]
Corresponding Author of This Article
Dai Zhou, PhD, Full Professor, Post-doctoral Researcher, Changsha Hospital for Maternal and Child Health Care, Hunan Normal University, No. 416 Chengnan Road, Changsha 410000, Hunan Province, China. zhoudai@hunnu.edu.cn
Research Domain of This Article
Dentistry, Oral Surgery & Medicine
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research-article
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Zhang RQ, Chu WH, Bai JB, Lei YH, Zhou D. Selenoprotein P attenuates oxidative senescence and ferroptosis-associated lipid peroxidation in dental pulp stem cells through a FOXM1-dependent program. World J Stem Cells 2026; 18(6): 119118 [DOI: 10.4252/wjsc.119118]
World J Stem Cells. Jun 26, 2026; 18(6): 119118 Published online Jun 26, 2026. doi: 10.4252/wjsc.119118
Selenoprotein P attenuates oxidative senescence and ferroptosis-associated lipid peroxidation in dental pulp stem cells through a FOXM1-dependent program
Ruo-Qi Zhang, Wei-Hao Chu, Jun-Bo Bai, Yong-Hua Lei, Dai Zhou
Ruo-Qi Zhang, Yong-Hua Lei, Department of Orthodontics and Prosthodontics, Center of Stomatology, Central South University, Changsha 410000, Hunan Province, China
Wei-Hao Chu, Jun-Bo Bai, School of Stomatology, Hunan University of Chinese Medicine, Changsha 410000, Hunan Province, China
Dai Zhou, Changsha Hospital for Maternal and Child Health Care Affiliated to Hunan Normal University, Changsha 410000, Hunan Province, China
Co-corresponding authors: Yong-Hua Lei and Dai Zhou.
Author contributions: Zhou D and Lei YH conceived and designed the research, edited and revised the manuscript; they contributed equally to this manuscript and are co-corresponding authors; Zhang RQ, Chu WH, and Bai JB performed experiments; Zhang RQ and Chu WH analyzed data; Zhang RQ, Lei YH, and Zhou D interpreted experimental results; Zhang RQ prepared figures and drafted the manuscript. All authors approved the final version of the manuscript.
Supported by the National Natural Science Foundation of China, No. 82201771; Natural Science Foundation of Hunan Province, No. 2024JJ6083; Health Research Project of Hunan Provincial Health Commission, No. W20243143; and Natural Science Foundation of Changsha, No. kq2202491.
Institutional review board statement: This study was conducted in accordance with the Declaration of Helsinki, reviewed and approved by the Medical Ethics Review Committee of Xiangya Hospital Central South University (Approval No. 2025122275). Informed consent was obtained from all participants or their legal guardians.
Conflict-of-interest statement: The authors report no relevant conflicts of interest for this article.
Data sharing statement: The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.
Corresponding author: Dai Zhou, PhD, Full Professor, Post-doctoral Researcher, Changsha Hospital for Maternal and Child Health Care, Hunan Normal University, No. 416 Chengnan Road, Changsha 410000, Hunan Province, China. zhoudai@hunnu.edu.cn
Received: January 20, 2026 Revised: February 21, 2026 Accepted: April 2, 2026 Published online: June 26, 2026 Processing time: 157 Days and 2.2 Hours
Core Tip
Core Tip: Aging-associated decline of dental pulp stem cells is linked to impaired selenium-dependent antioxidant defense. This study integrates single-cell transcriptomics, oxidative stress modeling, and human tissue validation to show that selenoprotein P and sodium selenite co-treatment reduces senescence and ferroptosis-associated lipid peroxidation in dental pulp stem cells. The combined treatment is more effective than either agent alone, and ferrostatin-1 rescue supports ferroptosis-related injury involvement. Transcriptomic and knockdown analyses identify a forkhead box protein M1-dependent protective program downstream of selenoprotein P/selenium support, highlighting a candidate strategy for preserving dental pulp vitality during aging.
