Mitochondria are highly dynamic organelles in continuous fusion and fission processes in response to various cellular stress. Mitochondrial dynamics, including mitochondrial fission/fusion and turnover, are important for the mitochondrial quality control. An imbalance between mitochondrial fission and fusion has been shown to contribute to many pathologies including ischemia/reperfusion (I/R) injury. Previous studies have shown that during the reperfusion period mitochondria undergo fission and that there is absence or reduction in mitochondrial fusion. Mitochondria fission renders cells highly susceptible to mitochondrial permeability transition pore (mPTP) opening, leading to an activation of the apoptotic pathway during reperfusion period. Pharmacological modulation of mitochondrial dynamics may have protective effects against I/R injury. Recently, we found that treatment of human umbilical vein endothelial cells with a small molecule, LPTC could significantly increase the percentage of cells containing tubular mitochondria and reduced cell death after simulated I/R. Furthermore, we demonstrated that LPTCcould restore tubular network in response to genetically induced mitochondrial fragmentation in the Mfn1 knockout (Mfn1-/-) and Mfn2 knockout (Mfn 2-/-) MEF cells. Our data showed that pharmacological modulation of mitochondrial fission/fusion by LPTC had an anti-apoptotic effect in the I/R experimental models.

Roles of mitochondrial fusion promoter in ischemia/reperfusion injury

256th National Meeting (2018)

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