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In AP, particularly in severe forms associated with microcirculatory impairment, HIF-1α stabilization may support glycolytic adaptation but can also accompany inflammatory activation and pathological autophagy ( Taken together, mitochondria and the nucleus form a tightly coupled signaling axis in which mitochondrial dysfunction in AP activates nuclear regulators such as NF-κB, ATF4, p53, NRF2, and HIF-1α, thereby influencing inflammation, autophagy, antioxidant defense, and cell-death pathways ( 3.5 Mitochondria and lipid droplets Metabolic adaptation to this stress also depends on how mitochondria interface with lipid-handling organelles
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