Static Magnetic Fields Exposure Allievates Liver Injury via Promoting Ca 2+ Influx and Cellular Respiration [scRNA-Seq]

Magnetic fields influence a wide range of biological processes, from animal navigation to human cellular metabolism. Despite these diverse effects, the therapeutic mechanisms of static magnetic fields (SMFs) remain poorly understood. Here we show that SMFs exposure markedly ameliorates drug-induced liver injury in mice, including both acetaminophen- and CCl4-induced models. SMFs treatment reduced serum aminotransferases, limited collagen deposition, and improved hepatocyte survival in vitro and in vivo. Multi-omics analyses revealed pronounced metabolic reprogramming, characterized by enhanced ATP production, increased oxygen consumption, and elevated mitochondrial membrane potential. These findings indicate that SMFs promote cellular respiration and stabilize hepatic energy homeostasis under injury conditions. At the mechanistic level, SMFs increased intracellular Ca2+ influx via activation of the Piezo1 channel and enhanced malate–aspartate shuttle activity through malate dehydrogenase 1 (MDH1). Together, our study establishes SMFs as a potent modulator of hepatocyte metabolism and highlights their promise as a non-invasive therapeutic strategy for liver disease.