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Publications

Journal Article Epublish

PubMed: 40640387 DOI: 10.1038/s41598-025-09077-w

Field direction of static magnetic fields influences kidney fibrosis progression through MAPK signaling and cell cycle alteration.

Sci Rep 15(1):24841

Authors: Seong Min Lee, Saram Lee, Kyu Hyeon Kim, Daehan Kim, Seong Joon Park, Kyu Hong Kim, Sunhwa Lee, Eunjin Bae, Kyung Don Yoo, Jae Wook Lee, Joong Yull Park, Yon Su Kim, Ran-Hui Cha, Seung Hee Yang

Affiliations

  • Department of Biomedical Sciences, Seoul National University, Seoul, Republic of Korea.
  • Department of Transdisciplinary Medicine, Seoul National University Hospital, Seoul, Republic of Korea. Department of Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea. Innovative Medical Technology Research Institute, Seoul National University Hospital, Seoul, Republic of Korea.
  • Department of Medical Engineering, Graduate School, Chung-Ang University, Seoul, Republic of Korea.
  • Division of Nephrology, Department of Internal Medicine, Kangwon National University Hospital, Chuncheon, Republic of Korea.
  • Institute of Medical Science, College of Medicine, Gyeongsang National University, Jinju, Republic of Korea.
  • Department of Internal Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Republic of Korea.
  • Nephrology Clinic, National Cancer Center of Korea, Goyang, Republic of Korea.
  • Department of Internal Medicine, Seoul National University Hospital, Seoul, Republic of Korea. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea. Department of Kidney Research Institute, Seoul National University Medical Research Center, Seoul, Republic of Korea.
  • Biomedical Research Institute, Seoul National University Hospital, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea. Division of Nephrology, Department of Internal Medicine, National Medical Center, Seoul, Republic of Korea.
  • Department of Kidney Research Institute, Seoul National University Medical Research Center, Seoul, Republic of Korea. Biomedical Research Institute, Seoul National University Hospital, 101, Daehak-ro, Jongno-gu, Seoul, Republic of Korea.

Abstract

Various mechanisms, including inflammation, oxidative stress, and apoptosis, are involved in the transition from acute kidney injury to chronic kidney disease (AKI-to-CKD). In this study, we aimed to determine the pathway linking acute injury and fibrosis under static magnetic fields (SMFs). Human tubular epithelial cells (hTECs) were cultured on SMF platforms (119 mT; outward vs. inward direction) for 3 days, followed by treatment with adenine and p38 mitogen-activated protein kinase (MAPK) inhibitor to verify the role of MAPK pathway. In-vivo, mice were orally administered adenine (2mg/mouse/day) for 14 days to induce tubular injury, and p38 MAPK inhibitor (iP38, 10mg/kg) was injected intraperitoneally to evaluate its therapeutic effect. Inward SMF exposure significantly increased phospho-p38 (pp38) expression compared to outward SMFs. p38 MAPK inhibition reduced G1/S arrest and oxidative stress, apoptosis, and expression of fibrosis markers under inward SMFs. Additionally, iP38 treatment alleviated inflammation and fibrosis in adenine-induced tubular nephropathy (AITN). This study revealed that SMF-related AKI-to-CKD transition progresses with the direction of SMFs affecting the severity of injury, whereas p38 MAPK inhibition attenuates SMF-induced kidney injury and prevents fibrosis.

MeSH

Cells, Fibrosis, P38 Mitogen-Activated Protein Kinases, Stress, Physiological, Kidney, Oxidative Stress, Therapeutics, Apoptosis, Adenine, Cell Cycle