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Mitochondrial fission factor (MFF) is a tail-anchored membrane protein localized to the mitochondrial outer membrane and peroxisomes[1][2][4][5]. MFF is essential for the recruitment of dynamin-related protein 1 (Drp1/DNM1L), a GTPase that mediates mitochondrial and peroxisomal fission[4][5]. Loss or suppression of MFF leads to elongated, interconnected mitochondrial networks, while overexpression causes mitochondrial fragmentation[2][4]. Its role is critical for cellular apoptosis, energy homeostasis, and adaptation to stress. Malfunction or dysregulation of MFF has been implicated in cancer, neurodegeneration (such as Huntington’s and Alzheimer’s diseases), cardiovascular, and metabolic disorders. Although not currently a direct drug target, modulation of MFF-related fission pathways represents an area of emerging therapeutic interest[4][5][6].
Inhibition or activation of mitochondrial fission via modulation of MFF-Drp1 interaction (potential mechanism for future drugs); Alteration of mitochondrial morphology by influencing recruitment of Drp1 to mitochondria; Modulation of apoptosis pathways through control of cytochrome c release.
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