Mitochondria elongation is mediated through SIRT1-mediated MFN1 stabilization

Oanh, Nguyen Thi Kim; Park, Yong-Yea; Cho, Hyeseong

doi:10.1016/j.cellsig.2017.06.019

Cited by 48 publications

(32 citation statements)

References 33 publications

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“…Notably, melatonin may directly reduce diabetic renal damage by sustaining mitochondrial homeostasis. This notion has been supported by ample evidence, which has documented the role of melatonin in mitochondrial protection (27,64,65). Melatonin suppresses excessive mitochondria fission (19), reverses protective mitophagy (24), scavenges mitochondrial ROS (66), alleviates mitochondrial calcium overload (18,67), sustains mitochondrial energy metabolism (68), modifies mitochondrial sirtuin protein (69) and blocks the caspase-9 apoptosis pathway (61,70).…”

Section: Discussionmentioning

confidence: 99%

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Melatonin attenuates renal fibrosis in diabetic mice by activating the AMPK/PGC1α signaling pathway and rescuing mitochondrial function

Yan

et al. 2018

Mol Med Report

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Mitochondrial homeostasis is a highly regulated process that serves a critical role in the maintenance of renal structure and function. The growing interest in the field of mitochondrial homeostasis promises to provide more information regarding the mechanisms involved in diabetic renal fibrosis, and aid in the development of novel strategies to combat the disease. In the present study, the effects of melatonin on renal damage in mice with diabetes were evaluated and the underlying mechanisms were investigated.

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Section: Discussionmentioning

confidence: 99%

“…Sample preparation and histological analysis. The kidneys were harvested, fixed for 1 h in 4% (w/v) paraformaldehyde at room temperature, and rapidly frozen in Optimal Cutting Temperature Compound (Agar Scientific, Ltd., Stansted, UK) for the preparation of cryosections (size, 4 µm) (27). Hematoxylin and eosin (H&E), Masson's trichrome (cat.…”

Section: Methodsmentioning

confidence: 99%

Melatonin attenuates renal fibrosis in diabetic mice by activating the AMPK/PGC1α signaling pathway and rescuing mitochondrial function

Yan

et al. 2018

Mol Med Report

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“…Furthermore, previous studies have reported that Tan IIA may regulate tumor development associated with osteosarcoma (57), as well as gastric (58), lung (59), esophageal (60) and prostate (61) cancers. Functional assays demonstrated that Tan IIA may inhibit cancer proliferation, suppress tumor growth, reduce cancer migration and enhance the apoptosis of cancer cells (62). In addition, it has been demonstrated that Tan IIA inhibits epithelial-mesenchymal transition via signal transducer and activator of transcription 3 signaling (16), suppresses β-catenin/vascular endothelial growth factor-mediated angiogenesis (63), and enhances cellular apoptosis via phosphatase and tensin homolog-mediated inhibition of the phosphoinositide 3-kinase/protein kinase B pathway (64).…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA regulates colorectal cancer apoptosis via attenuation of Parkin‑mediated mitophagy by suppressing AMPK/Skp2 pathways

Ke-bo

2018

Mol Med Report

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Mitophagy is important for cancer development. Notably, the role of Parkin‑mediated mitophagy in colorectal cancer (CRC) mortality has not been fully determined. Therefore, the present study aimed to investigate the effect of Parkin‑mediated mitophagy on CRC apoptosis. In addition, the present study investigated the therapeutic effects of Tanshinone IIA (Tan IIA) on the regulation of CRC cell death via mitophagy. Cellular apoptosis was measured following Tan IIA treatment. In addition, mitophagy activity was evaluated by immunofluorescence and western blotting. The results of the present study revealed that Tan IIA may enhance CRC cell death. In addition, the results demonstrated that Tan IIA enhanced mitochondrial apoptosis, as demonstrated by reduced mitochondrial membrane potential, elevated mitochondrial permeability transition pore opening, and increased oxidative stress, mitochondrial energy disorder and proapoptotic factor expression. Furthermore, the results of the present study demonstrated that Tan IIA induced mitochondrial apoptosis via inhibition of mitophagy. In addition, it was revealed that mitophagy could suppress mitochondrial apoptosis. Functional assays revealed that Tan IIA suppressed the adenosine monophosphate‑activated protein kinase (AMPK) pathway, resulting in the inactivation of S‑phase kinase associated protein 2 (Skp2). Furthermore, reduced levels of Skp2 failed to activate Parkin, thus resulting in inhibition of mitophagy. Conversely, reactivation of AMPK and overexpression of Skp2 rescued mitophagy activity and thus attenuated the Tan IIA‑induced apoptosis of CRC cells. In conclusion, the results of the present study demonstrated the beneficial role of mitophagy in CRC cell survival and suggested that Tan IIA may be an effective therapeutic agent, which suppresses mitophagy activity and enhances CRC apoptosis.

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“…Scientific, Inc.) according to the manufacturer's protocol (Oanh, Park, & Cho, 2017). Null vector transfection was used as the control group (Ad-ctrl).…”

Section: Mem Media Supplemented With Lipofectamine 2000 (Thermo Fishermentioning

confidence: 99%

DUSP1 recuses diabetic nephropathy via repressing JNK‐Mff‐mitochondrial fission pathways

Sheng

Dai

et al. 2018

Journal Cellular Physiology

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Excessive mitochondrial fission has been identified as the pathogenesis of diabetic nephropathy (DN), although the upstream regulatory signal for mitochondrial fission activation in the setting of DN remains unknown. In the current study, we found that dual-specificity protein phosphatase-1 (DUSP1) was actually downregulated by chronic hyperglycemia stimulus. Lower DUSP1 expression was associated with glucose metabolism disorder, renal dysfunction, kidney hypertrophy, renal fibrosis, and glomerular apoptosis. At the molecular level, defective DUSP1 expression activated JNK pathway, and the latter selectively opened mitochondrial fission by modulating mitochondrial fission factor (Mff) phosphorylation. Excessive Mff-related mitochondrial fission evoked mitochondrial oxidative stress, promoted mPTP opening, exacerbated proapoptotic protein leakage into the cytoplasm, and finally initiated mitochondria-dependent cellular apoptosis in the setting of diabetes. However, overexpression of DUSP1 interrupted Mff-related mitochondrial fission, reducing hyperglycemia-mediated mitochondrial damage and thus improving renal function. Overall, we have shown that DUSP1 functions as a novel malefactor in diabetic renal damage that mediates via modifying Mff-related mitochondrial fission. Thus, finding strategies to regulate the balance of the DUSP1-JNK-Mff signaling pathway and mitochondrial homeostasis may be a therapeutic target for treating diabetic nephropathy in clinical practice.

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Mitochondria elongation is mediated through SIRT1-mediated MFN1 stabilization

Cited by 48 publications

References 33 publications

Melatonin attenuates renal fibrosis in diabetic mice by activating the AMPK/PGC1α signaling pathway and rescuing mitochondrial function

Melatonin attenuates renal fibrosis in diabetic mice by activating the AMPK/PGC1α signaling pathway and rescuing mitochondrial function

Tanshinone IIA regulates colorectal cancer apoptosis via attenuation of Parkin‑mediated mitophagy by suppressing AMPK/Skp2 pathways

DUSP1 recuses diabetic nephropathy via repressing JNK‐Mff‐mitochondrial fission pathways

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