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Field direction of static magnetic fields influences kidney fibrosis progression through MAPK signaling and cell
Seong Min Lee1, Saram Lee2,3,4, Kyu Hyeon Kim1
1Department of Biomedical Sciences, Seoul National University, 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.
Insights
Static magnetic fields (SMFs) can worsen acute kidney injury to chronic kidney disease (AKI-to-CKD) transition. P38 mitogen-activated protein kinase (MAPK) inhibition mitigates SMF-induced kidney damage and fibrosis.
Area of Science:
- Nephrology
- Biophysics
- Cell Biology
Background:
- The transition from acute kidney injury to chronic kidney disease (AKI-to-CKD) involves complex mechanisms like inflammation, oxidative stress, and apoptosis.
- Static magnetic fields (SMFs) are increasingly studied for their biological effects, but their role in kidney injury progression remains unclear.
Purpose of the Study:
- To investigate the pathway linking acute kidney injury and fibrosis under static magnetic fields (SMFs).
- To determine the influence of SMF direction on kidney injury progression.
- To evaluate the therapeutic potential of p38 mitogen-activated protein kinase (MAPK) inhibition in mitigating SMF-induced kidney damage.
Main Methods:
- Human tubular epithelial cells (hTECs) were exposed to inward and outward directed SMFs (119 mT).
- Adenine was used to induce tubular injury in vivo in mice, followed by p38 MAPK inhibitor (iP38) treatment.
- Key markers of cell cycle arrest, oxidative stress, apoptosis, inflammation, and fibrosis were assessed.
Main Results:
- Inward SMF exposure significantly increased phospho-p38 (pp38) expression compared to outward SMFs.
- p38 MAPK inhibition reduced G1/S arrest, oxidative stress, apoptosis, and fibrosis markers under inward SMFs.
- iP38 treatment alleviated inflammation and fibrosis in adenine-induced tubular nephropathy (AITN) in mice.
Conclusions:
- The direction of SMFs influences the severity of kidney injury and progression to fibrosis.
- p38 MAPK pathway is a critical mediator in SMF-induced kidney injury.
- p38 MAPK inhibition demonstrates therapeutic potential in attenuating SMF-related kidney injury and preventing fibrosis.
