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Triggering of a neutrophil by either PMA or fMLP leads to the phosphorylation of P47phox, a cytosolic subunit of NADPH complex and translocate to the plasma membrane to interact with flavocytochrome b558 [71,72,73]

Recent evidence has revealed mitochondrial dysfunction in RA PBMCs, involving reduced ATP, disrupted m, elevated ROS, and upregulated ROMO1/OMA1 expression ( 2 O 2 -induced) upregulates MST1 expression in RA-FLSs, triggering mitochondrial dysfunction and apoptosis ( Taken together, mitochondrial metabolism reprogramming not only plays a key role in RA pathophysiology, but may be a promising potential target for future treatment of RA

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