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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Stem Cells. Aug 26, 2026; 18(8): 119568
Published online Aug 26, 2026. doi: 10.4252/wjsc.119568
Letter to the Editor: Epiregulin-EGFR-ERK1/2 signaling as a therapeutic axis for rescuing mesenchymal stem cell dysfunction in inflammatory periodontal niches
Kruthika Prakash, Kandasamy Nagarajan ArulJothi, Ramya Lakshmi Rajendran, Prakash Gangadaran, Byeong-Cheol Ahn
Kruthika Prakash, Kandasamy Nagarajan ArulJothi, Department of Genetic Engineering, SRM Institute of Science and Technology, Kattankulathur 603203, Tamil Nādu, India
Ramya Lakshmi Rajendran, Byeong-Cheol Ahn, BK21 FOUR KNU Convergence Educational Program of Biomedical Sciences for Creative Future Talents, Department of Biomedical Sciences, School of Medicine, Kyungpook National University, Daegu 41944, South Korea
Ramya Lakshmi Rajendran, Prakash Gangadaran, Byeong-Cheol Ahn, Department of Nuclear Medicine, School of Medicine, Kyungpook National University, Daegu 41944, South Korea
Ramya Lakshmi Rajendran, Prakash Gangadaran, Byeong-Cheol Ahn, Cardiovascular Research Institute, Kyungpook National University, Daegu 41944, South Korea
Byeong-Cheol Ahn, Department of Nuclear Medicine, Kyungpook National University Hospital, Daegu 41944, South Korea
Co-first authors: Kruthika Prakash and Kandasamy Nagarajan ArulJothi.
Co-corresponding authors: Prakash Gangadaran and Byeong-Cheol Ahn.
Author contributions: Prakash K, ArulJothi KN, Rajendran RL, Gangadaran P, and Ahn BC designed the overall concept and outline of the manuscript, contributed to the discussion and design of the manuscript, the writing and editing of the manuscript, illustrations, and review of the literature. Prakash K and ArulJothi KN served as co-first authors and contributed equally. Gangadaran P and Ahn BC served as co-corresponding authors and contributed equally to the supervision, critical revision, and final approval of the manuscript.
Supported by Basic Science Research Program Through the National Research Foundation of Korea, No. NRF-2022R1I1A1A01068652.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Byeong-Cheol Ahn, MD, PhD, Department of Nuclear Medicine, School of Medicine, Kyungpook National University, 680, Gukchaebosang ro, Jung gu, Daegu 41944, South Korea. abc2000@knu.ac.kr
Received: February 2, 2026
Revised: March 29, 2026
Accepted: May 8, 2026
Published online: August 26, 2026
Processing time: 202 Days and 0.4 Hours
Abstract

Periodontitis is a highly prevalent chronic inflammatory disease characterized by progressive destruction of periodontal supporting tissues and remains difficult to treat due to inflammation-induced impairment of regenerative responses. Persistent inflammatory niches suppress mesenchymal stem cell function, limiting the effectiveness of current regenerative therapies. Therefore, identifying factors that restore stem cell activity under inflammatory conditions is of significant clinical importance. We read with interest the study by Zhao et al entitled “Epiregulin enhances periodontal tissue regeneration by promoting bone marrow mesenchymal stem cell functions under inflammatory niches”. This article highlights the regenerative potential of epiregulin, which enhances bone marrow mesenchymal stem cell proliferation, migration, and osteogenic differentiation under inflammatory stress by activating the epidermal growth factor receptor-extracellular signal-regulated kinase signaling pathway, thereby promoting periodontal bone regeneration.

Keywords: Epiregulin; Mesenchymal stem cells; Periodontitis; Inflammatory niche; Epidermal growth factor receptor-extracellular signal-regulated kinase signaling

Core Tip: Epiregulin restores inflammation-impaired bone marrow mesenchymal stem cell function via epidermal growth factor receptor-extracellular signal-regulated kinase signaling, highlighting its potential as a promising therapeutic target for periodontal regeneration under inflammatory conditions. By activating this pathway, epiregulin rescues key stem cell functions, including proliferation, migration, and osteogenic differentiation, that are suppressed by inflammatory stimuli such as tumor necrosis factor-alpha, offering a mechanistically driven and inflammation-resilient strategy for periodontal tissue regeneration and clinical translation.

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