CORRECTION article
Front. Physiol.
Sec. Exercise Physiology
Volume 16 - 2025 | doi: 10.3389/fphys.2025.1661262
This article is part of the Research TopicPhysiological and Pathological Responses to Hypoxia and High Altitude, Volume IIIView all 15 articles
Correction: Exercise preconditioning alleviates photothrombotic ischemic stroke in mice by orchestrating neutrophils
Provisionally accepted
Tae Yeon Kim1
Yun Seo Cho1
Jae Yeon Park1Songwon Woo1
Kihoon Yuk1Dong Heon Yi1In cheol Jeong2,3
Jin Pyeong Jeon4
Yoe-Sik Bae5Min-Chul Lee6
Hyo Youl Moon1*- 1Seoul National University, Seoul, Republic of Korea
- 2Icahn School of Medicine at Mount Sinai, New York, United States
- 3Hallym University, Chuncheon-si, Republic of Korea
- 4Hallym University College of Medicine, Chuncheon-si, Republic of Korea
- 5Sungkyunkwan University, Suwon, Republic of Korea
- 6CHA University, Pocheon-si, Republic of Korea
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Background: In ischemic stroke (IS) pathology, neutrophils are rapidly recruited to the infarcted brain and exacerbate tissue damage by releasing the amount of neutrophil extracellular traps (NETs). Previous studies have demonstrated that alleviating IS is associated with reduced accumulated neutrophils and NET levels. Notably, exercise preconditioning (EP) has the potential to modulate neutrophil function, thereby contributing to the amelioration of IS. This study compared the functional differences between resting and EP-induced neutrophils under IS pathology. Methods: Eight-week-old C57BL/6J male mice underwent 8 weeks of voluntary exercise before photothrombotic ischemic stroke (PTI) surgery. Behavioral tests were conducted 2 days after PTI to verify the effects of EP on acute recovery following PTI. To evaluate whether EP affected neutrophil recruitment and chemotactic signaling, RT-qPCR was performed on infarcted cortical regions. A migration assay was performed to assess the migration capacity of blood-isolated neutrophils under IS. Plasma NET levels were quantified using enzyme-linked immunosorbent assay (ELISA), while NET presence in the brain was evaluated through immunofluorescence (IF) staining. Results: Exercise-preconditioned-PTI (EP-PTI) mice showed superior behavioral outcomes in grip strength and open-field tests both before and 2 days after PTI compared to sedentary-PTI (Sed-PTI) mice. EP also suppressed the expression of chemotactic signaling molecules following PTI, suggesting reduced inflammatory recruitment and infiltration. Furthermore, EP reduced the migration capacity of neutrophils and decreased NET formations in both plasma and brain 2 days after PTI surgery. Conclusion: Our study demonstrates that EP enhances acute recovery in IS and may beneficially orchestrate IS pathology by inhibiting the migratory capacity and reducing NET formation in vivo.
Keywords: Exercise preconditioning, neutrophil extracellular traps, Migration capacity, photothrombotic ischemic stroke, voluntary exercise
Received: 07 Jul 2025; Accepted: 04 Aug 2025.
Copyright: © 2025 Kim, Cho, Park, Woo, Yuk, Yi, Jeong, Jeon, Bae, Lee and Moon. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Hyo Youl Moon, Seoul National University, Seoul, Republic of Korea
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.