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doi: 10.5483/BMBRep.2023-0098 Summary Keywords acute pancreatitis, mitochondrial, calcium overload, mitochondrial permeability transition pore, regulated cell death Citation Chen F, Xu K, Han Y, Ding J, Ren J, Wang Y, Ma Z and Cao F (2024) Mitochondrial dysfunction in pancreatic acinar cells: mechanisms and therapeutic strategies in acute pancreatitis

Phosphocreatine (5-40 mM, 24 h) at different concentrations might contribute to protection of the NRK-52E cells against MGO-induced kidney injury [4]

These findings have significant implications for developing supportive care protocols that reduce long-term chemotherapy side effects and improve quality of life for cancer survivors

75 These findings reinforce the notion that, rather than initiating dopaminergic cell death, inflammation may perpetuate it, thus contributing to Parkinson's disease progression