2018
DOI: 10.1016/j.bcp.2018.01.038
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Activation of mitochondrial fusion provides a new treatment for mitochondria-related diseases

Abstract: Mitochondria fragmentation destabilizes mitochondrial membranes, promotes oxidative stress and facilitates cell death, thereby contributing to the development and the progression of several mitochondria-related diseases. Accordingly, compounds that reverse mitochondrial fragmentation could have therapeutic potential in treating such diseases. BGP-15, a hydroxylamine derivative, prevents insulin resistance in humans and protects against several oxidative stress-related diseases in animal models. Here we show th… Show more

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Cited by 73 publications
(52 citation statements)
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“…Observations published recently suggest that BGP-15 affects mitochondrial fusion-fission cycle, preventing mitochondrial fragmentation [23]. In accordance with these observations, BGP-15 administration results in a decrease in the number of damaged mitochondria as it has been demonstrated in our recent study, which is accompanied with the increase in mitophagy.…”
Section: Discussionsupporting
confidence: 92%
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“…Observations published recently suggest that BGP-15 affects mitochondrial fusion-fission cycle, preventing mitochondrial fragmentation [23]. In accordance with these observations, BGP-15 administration results in a decrease in the number of damaged mitochondria as it has been demonstrated in our recent study, which is accompanied with the increase in mitophagy.…”
Section: Discussionsupporting
confidence: 92%
“…Its various experimental effects have been demonstrated in a series of different animal models and also in cell cultures. These are protective effects influencing among others heart, skeletal muscle, liver, oocytes, skin and show the involvement of mitochondria [5,[18][19][20][21][22][23][24]. Hindrance of ROS elevation and also moderation in JNK activation by BGP-15 have been shown in different experimental models [18].…”
Section: Introductionmentioning
confidence: 99%
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“…This cell line is a suitable in vitro model for the investigation of glucose uptake [29]. To evaluate the effect of BGP-15 on mitochondrial fragmentation, WRL-68, C 2 C 12 , A549 and Sf9 cell cultures were maintained [30]. Mitochondrial ROS production has also been studied on the WRL-68 cell line [24].…”
Section: Cell Culture Modelsmentioning
confidence: 99%
“…Therefore, therapies oriented to enhance mitochondrial fusion or prevent fission might be beneficial to attenuate hypertension-induced organ damage. Indeed, hydroxylamine derivatives, which activate optic atrophy-1 and promote the fusion of inner mitochondrial membranes, ameliorated lung damage in a murine model of pulmonary arterial hypertension [51]. Recently, treatment with a drug that prevents activation of the mitochondrial fission marker dynamin related protein (DRP)-1 ameliorated vascular remodeling and inflammation in spontaneously hypertensive rats [52], in accordance with previous observations in cardiomyocytes subjected to renal [53] and cardiac [54] reperfusion injury.…”
Section: Mechanisms Of Mitoprotectionmentioning
confidence: 99%