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Overall, these findings indicate that mitochondrial Ca 2+ overload in diabetic platelets is not an isolated defect but the downstream consequence of coordinated dysregulation across influx pathways (SOCE, TRPC6, reverse-mode NCX), clearance systems (PMCA and SERCA impairment), redox-sensitive signaling axes (RAGE-PKC), and inhibitory pathways (cAMP and NO-sGC-cGMP)
Other Biological Oxidations Oxidase complexes, like cytochrome oxidase, transfer electrons directly from NADH and other substrates to oxygen, producing water
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