A reciprocal relationship between reactive oxygen species and mitochondrial dynamics in neurodegeneration

Hung, Clara Hiu Ling; Cheng, Sally Shuk Yee; Cheung, Yiu Wing; Wuwongse, S; Zhang, Natalie Qishan; Ho, Yuen Shan; Lee, Simon Ming‐Yuen; Chang, Raymond Chuen‐Chung

doi:10.1016/j.redox.2017.08.010

Cited by 130 publications

(92 citation statements)

References 76 publications

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“…TICAE and TICAE-ROSI cells had similar mitochondrial areas per cell in the sham condition, but it increased in irradiated TICAE-ROSI cells. Mitochondrial circularity was statistically different between the cell types and treatment conditions, of which high mitochondrial circularity is associated with a high redox stress state (Ahmad et al, 2013;Hung et al, 2018).…”

Section: Irradiation Triggers Mitochondrial Remodeling In Endothelialmentioning

confidence: 95%

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

et al. 2020

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Background and Purpose: Up to 50-60% of all cancer patients receive radiotherapy as part of their treatment strategy. However, the mechanisms accounting for increased vascular risks after irradiation are not completely understood. Mitochondrial dysfunction has been identified as a potential cause of radiation-induced atherosclerosis.Materials and Methods: Assays for apoptosis, cellular metabolism, mitochondrial DNA content, functionality and morphology were used to compare the response of endothelial cells to a single 2 Gy dose of X-rays under basal conditions or after pharmacological treatments that either reduced (EtBr) or increased (rosiglitazone) mitochondrial content.Results: Exposure to ionizing radiation caused a persistent reduction in mitochondrial content of endothelial cells. Pharmacological reduction of mitochondrial DNA content rendered endothelial cells more vulnerable to radiation-induced apoptosis, whereas rosiglitazone treatment increased oxidative metabolism and redox state and decreased the levels of apoptosis after irradiation.Conclusion: Pre-existing mitochondrial damage sensitizes endothelial cells to ionizing radiation-induced mitochondrial dysfunction. Rosiglitazone protects endothelial cells from the detrimental effects of radiation exposure on mitochondrial metabolism and oxidative stress. Thus, our findings indicate that rosiglitazone may have potential value as prophylactic for radiation-induced atherosclerosis.

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Section: Irradiation Triggers Mitochondrial Remodeling In Endothelialmentioning

confidence: 95%

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

et al. 2020

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“…Interestingly, studies investigating mitochondrial network dynamics have found that the state of mitochondrial morphology, whether fused or fragmented, has a direct consequence on all of the above-mentioned mitochondrial functions. Mitochondrial dynamics themselves undergo alterations with age [20][21][22][23][24][25]. Studies in nematodes [26], flies [27], and mice [28] have shown that the mitochondrial network of aged animals is often more heterogeneous, fragmented, and comprised of large, swollen mitochondria that cannot be eliminated by mitophagy.…”

Section: Introductionmentioning

confidence: 99%

Causal roles of mitochondrial dynamics in longevity and healthy aging

et al. 2019

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Mitochondria are organized in the cell in the form of a dynamic, interconnected network. Mitochondrial dynamics, regulated by mitochondrial fission, fusion, and trafficking, ensure restructuring of this complex reticulum in response to nutrient availability, molecular signals, and cellular stress. Aberrant mitochondrial structures have long been observed in aging and age‐related diseases indicating that mitochondrial dynamics are compromised as cells age. However, the specific mechanisms by which aging affects mitochondrial dynamics and whether these changes are causally or casually associated with cellular and organismal aging is not clear. Here, we review recent studies that show specifically how mitochondrial fission, fusion, and trafficking are altered with age. We discuss factors that change with age to directly or indirectly influence mitochondrial dynamics while examining causal roles for altered mitochondrial dynamics in healthy aging and underlying functional outputs that might affect longevity. Lastly, we propose that altered mitochondrial dynamics might not just be a passive consequence of aging but might constitute an adaptive mechanism to mitigate age‐dependent cellular impairments and might be targeted to increase longevity and promote healthy aging.

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“…Fragmented mitochondria can be degraded selectively by mitophagy to protect the cell from apoptosis. Granular (fragmented) mitochondria are linked to high levels in ROS, and tubular (filamentous) mitochondria are inversely proportional to ROS level in neurodegeneration [73]. During mitosis, the question of whether fragmented mitochondria produce H 2 O 2 more than filamentous mitochondria should be addressed.…”

Section: Source For H 2 O 2 Generation Throughout the Cell Cyclementioning

confidence: 99%

The Role of Hydrogen Peroxide and Peroxiredoxins throughout the Cell Cycle

Heo¹,

Kim²,

Kang³

2020

Antioxidants

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Hydrogen peroxide (H2O2) is an oxidizing agent that induces cellular damage at inappropriate concentrations and gives rise to an arrest during cell cycle progression, causing cell death. Recent evidence indicates that H2O2 also acts as a promoter for cell cycle progression by oxidizing specific thiol proteins. The intracellular concentration of H2O2 is regulated tightly, enabling its use as a cellular signaling molecule while minimizing its potential to cause cellular damage. Peroxiredoxins (Prxs) have peroxidase activity toward H2O2, organic hydroperoxides, and peroxynitrite for protecting cells from oxidative stress. They are suggested to work as signaling mediators, allowing the local accumulation of H2O2 by inactivating their peroxidase activity uniquely compared with other antioxidant proteins such as catalase and glutathione peroxidase. Given that Prxs are highly sensitive to oxidation by H2O2, they act as sensors and transducers of H2O2 signaling via transferring their oxidation state to effector proteins. The concentrations of intracellular H2O2 increase as the cell cycle progresses from G1 to mitosis. Here, we summarize the roles of Prxs with regard to the regulation of cell cycle-dependent kinase activity and anaphase-promoting complex/cyclosome in terms of changes in H2O2 levels. Protection of the cell from unwanted progression of the cell cycle is suggested to be a role of Prx. We discuss the possible roles of Prxs to control H2O2 levels.

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A reciprocal relationship between reactive oxygen species and mitochondrial dynamics in neurodegeneration

Cited by 130 publications

References 76 publications

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

Causal roles of mitochondrial dynamics in longevity and healthy aging

The Role of Hydrogen Peroxide and Peroxiredoxins throughout the Cell Cycle

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