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Specifically, M1 macrophages predominantly utilize glycolysis to sustain their pro-inflammatory functions, whereas M2 macrophages depend on fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) [14]

Collectively, SYK deficiency dysregulates AMPK/STAT3 signaling under metabolic stress, leading to impaired mitophagy, ROS accumulation, and accelerated intrinsic apoptosis in SCs

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In many patients with IC/PBS, these signaling pathways are found to be either dysfunctional or interrupted at some point during the diseases progression (Hanno and Dmochowski, 2009