“…This mechanism complements the function of SLC25A51 and SLC25A52 carriers to transport NAD + into the mitochondria to support complex I activity [ [76] , [77] , [78] ]. In keeping with this notion, a decreased expression of SLC25A1 mRNA [ 79 ] or inhibition of its function by CTPI-2 drives mitochondrial dysfunction and OCR drop [ 80 ]. The reduction of NOX-dependent ROS production by CTPI-2 confirms that citrate export and the ensuing decarboxylation of malate by ME1 yields NADPH to generate NOX-dependent ROS for fungal killing.…”