A temporal study on NF-κB-mediated autonomous inflammatory response in iPSC-CMs induced by microwave radiation
Ecotoxicology and Environmental Safety, 2025
Zhang C., Deng W., Wang Y., Yao B., Dong J., Liu Z., Wang H., Xu X., Peng R., Zhang J.
| Disease area | Application area | Sample type | Products |
|---|---|---|---|
Environmental Health & Toxicology | Pathophysiology | Cell Culture Supernatant | Olink Target 96 |
Abstract
The study aims to explore the new mechanism of human induced pluripotent stem cell-derived myocardial cells (iPSC-CMs) damage caused by microwave exposure, focusing on the changes in inflammatory factors, and to clarify the association between the dynamic sensing network and electrophysiological disorders. In this study, iPSC-CMs were exposed to 60 W/kg S-band microwaves for 30 min. The damage effects and mechanisms were investigated 1 h, 3 h, and 6 h after radiation. Using techniques such as flow cytometry, transmission electron microscopy, calcium transient, Olink proteomics, and immunofluorescence, the activity, ultrastructure, calcium signal changes, and expression of inflammatory factors of iPSC-CMs after microwave radiation were detected. Results: After microwave radiation, the activity of iPSC-CMs significantly decreased, the mitochondrial cristae were broken, the Ca2 + activation time and activation speed were abnormal, the amplitude of calcium transient changed significantly, and the action potential repolarization was abnormal. The dynamic changes of inflammatory factors were as follows: 1 h after microwave radiation, IL-6 drove acute inflammatory response, 3 h when the NF-κB pathway integrated inflammatory signals through IL-8, and 6 h after, CXCL11 dominated the repair program, and VEGFA expression rebounded to synergistically promote generation. Microwave radiation activated the classical NF-κB pathway and regulated the inflammatory balance. This study found that microwave radiation caused structural and functional damage to iPSC-CMs, and the temporal inflammatory regulation is a new mechanism of injury.