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Mitochondrial fission process 1 protein (MTFP1) is an inner mitochondrial membrane GTPase central to the regulation of mitochondrial dynamics, especially maintaining the balance between fusion and fission. MTFP1 ensures mitochondrial network integrity and optimal bioenergetic function by stabilizing the inner membrane, supporting proper calcium handling, and limiting harmful reactive oxygen species levels. It is indispensable in tissues with high energy demand, such as heart muscle, where its deficiency leads to impaired mitochondrial structure, loss of bioenergetic efficiency, elevated proton leak, greater susceptibility to permeability transition pore opening, and, ultimately, progressive heart failure[1][2][3]. MTFP1’s emerging roles in cancer and metabolic adaptation suggest its dysfunction is of broad pathological relevance, making it a promising—though challenging—therapeutic target and a potential biomarker for mitochondrial and energy metabolism-related disorders[1]. Currently, there are no drugs directly targeting MTFP1 in clinical use, but it remains an active research interest for precision mitochondrial therapeutics.
For future therapies: Modulation of mitochondrial fusion/fission balance; Regulation of mitochondrial permeability transition pore (mPTP) sensitivity; Influence on ROS handling and cellular apoptosis susceptibility; No approved drugs yet provide clinical mechanism of action targeting MTFP1
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