Mitochondrial dysfunction as a bridge to pathology in acute pancreatitis: From molecular insights to novel therapeutic strategies

Figure 1 Mitochondrial structure and function in pancreatic acinar cells. Cyp D: Cyclophilin D; ANT: Adenine nucleotide translocation; mtDNA: Mitochondrial deoxyribonucleic acid; SERCA: Sarco/endoplasmic reticulum Ca²⁺-ATPases; PMCA: Plasma membrane Ca²⁺-ATPases.

Figure 2 The molecular mechanisms underlying mitochondrial dysfunction in acute pancreatitis. SOCE: Store-operated calcium entry; Cyp D: Cyclophilin D; ROS: Reactive oxygen species; MPTP: Mitochondrial permeability transition pore; IP3Rs: Inositol triphosphate receptors; RyRs: Ryanodine receptors; STIM1: Stromal interaction molecule 1; SERCA: Sarco/endoplasmic reticulum Ca²⁺-ATPases; OXPHOS: Oxidative phosphorylation; LC3: Microtubule-associated protein light chain 3; LAMP-2: Lysosome-associated membrane protein-2; PINK1: PTEN-induced putative kinase 1; FUNDC1: FUN14 domain containing 1; mtROS: Mitochondrial reactive oxygen species; mtDNA: Mitochondrial DNA; cGAS: Cyclic GMP-AMP synthase; STING: Stimulator of interferon genes; IRF7: Interferon regulatory factor 7; IRF3: Interferon regulatory factor 3.