Treadmill exercise attenuates cerebral ischaemic injury in rats by protecting mitochondrial function via enhancement of caveolin-1

Pan, Guoyuan; Zhang, Huimei; Zhu, Anqi; Lin, Yao; Zhang, Lili; Ye, Bingyun; Cheng, Jing-Yan; Shen, Wei-Min; Jin, Lingqin; Liu, Chan; Xie, Qipeng; Chen, Xiang

doi:10.1016/j.lfs.2020.118634

Cited by 9 publications

(3 citation statements)

References 44 publications

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“…Another potential mechanism through which Cav-1 works may occur through regulating Ca2+ influx, an intracellular event, which has been observed in tumor cells [ 56 ], endothelial [ 57 ], and smooth muscle cells [ 58 ], a process that may couple to mitochondrial resiliency as mitochondria can serve as a calcium sink in cells [ 59 ]. Similar effects were observed in a recently published study from Chen and colleagues that showed treadmill exercise protected mitochondrial integrity and inhibited endogenous mitochondrial-mediated apoptosis through Cav-1 upregulation [ 60 ]. These results demonstrate a key role in Cav-1 for maintaining mitochondria dynamics and further argue for the overexpression of neuronal Cav-1 as a potential therapeutic strategy to treat neurodegeneration diseases through preservation of mitochondrial function and dynamics.…”

Section: Discussionsupporting

confidence: 84%

Synapsin-Promoted Caveolin-1 Overexpression Maintains Mitochondrial Morphology and Function in PSAPP Alzheimer’s Disease Mice

Wang

Ichinomiya

Terada

et al. 2021

Cells

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Mitochondrial dysfunction plays a pivotal role in the Alzheimer’s Disease (AD) pathology. Disrupted mitochondrial dynamics (i.e., fusion/fission balance), which are essential for normal mitochondria structure and function, are documented in AD. Caveolin-1 (Cav-1), a membrane/lipid raft (MLR) scaffolding protein regulates metabolic pathways in several different cell types such as hepatocytes and cancer cells. Previously, we have shown decreased expression of Cav-1 in the hippocampus of 9-month (m) old PSAPP mice, while hippocampal overexpression of neuron-targeted Cav-1 using the synapsin promoter (i.e., SynCav1) preserved cognitive function, neuronal morphology, and synaptic ultrastructure in 9 and 12 m PSAPP mice. Considering the central role of energy production in maintaining normal neuronal and synaptic function and survival, the present study reveals that PSAPP mice exhibit disrupted mitochondrial distribution, morphometry, and respiration. In contrast, SynCav1 mitigates mitochondrial damage and loss and enhances mitochondrial respiration. Furthermore, by examining mitochondrial dynamics, we found that PSAPP mice showed a significant increase in the phosphorylation of mitochondrial dynamin-related GTPase protein (DRP1), resulting in excessive mitochondria fragmentation and dysfunction. In contrast, hippocampal delivery of SynCav1 significantly decreased p-DRP1 and augmented the level of the mitochondrial fusion protein, mitofusin1 (Mfn1) in PSAPP mice, a molecular event, which may mechanistically explain for the preserved balance of mitochondria fission/fusion and metabolic resilience in 12 m PSAPP-SynCav1 mice. Our data demonstrate the critical role for Cav-1 in maintaining normal mitochondrial morphology and function through affecting mitochondrial dynamics and explain a molecular and cellular mechanism underlying the previously reported neuroprotective and cognitive preservation induced by SynCav1 in PSAPP mouse model of AD.

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Section: Discussionsupporting

confidence: 84%

Synapsin-Promoted Caveolin-1 Overexpression Maintains Mitochondrial Morphology and Function in PSAPP Alzheimer’s Disease Mice

Wang

Ichinomiya

Terada

et al. 2021

Cells

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“… 38 More recent studies indicate that 8-week endurance training could inhibit non-alcoholic steatohepatitis-induced mitochondrial permeability transition pore opening, indicating decreased mitochondrial membrane permeability. 39 Seven days of treadmill exercise can prevent mitochondrial outer membrane permeabilization in the rat model of cerebral ischemic injury by increasing caveolin-1 expression, thus inhibiting excessive cytochrome C release from mitochondria, 40 reducing mitochondrial damage, and protecting mitochondrial integrity. In addition, 12 weeks of moderate-intensity treadmill exercise exerts cardioprotection in diabetic mice by down-regulating mammalian sterile 20-like kinase 1, which enhances mitochondrial membrane potential.…”

Section: Exercise Protects the Integrity Of Barriersmentioning

confidence: 99%

Exercise sustains the hallmarks of health

Qiu

Fernández‐García

Lehmann

et al. 2023

Journal of Sport and Health Science

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“…Treadmill exercise increased TOM20 expression through the Caveolin-1 pathway and maintained input signaling, thereby protecting mitochondrial integrity and activating the expression of mitochondrial transcription factors, activating mitochondrial biosynthesis, and reducing brain ischemia-induced injury [92,93]. Exercise induces a large number of mitochondrial adaptations in the muscle, including mitochondrial protein import.…”

Section: Exercise and Mitochondrial Protein Importmentioning

confidence: 99%

The Role of Exercise in Maintaining Mitochondrial Proteostasis in Parkinson’s Disease

Liu

et al. 2023

IJMS

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Parkinson’s disease (PD) is the second most common rapidly progressive neurodegenerative disease and has serious health and socio-economic consequences. Mitochondrial dysfunction is closely related to the onset and progression of PD, and the use of mitochondria as a target for PD therapy has been gaining traction in terms of both recognition and application. The disruption of mitochondrial proteostasis in the brain tissue of PD patients leads to mitochondrial dysfunction, which manifests as mitochondrial unfolded protein response, mitophagy, and mitochondrial oxidative phosphorylation. Physical exercise is important for the maintenance of human health, and has the great advantage of being a non-pharmacological therapy that is non-toxic, low-cost, and universally applicable. In this review, we investigate the relationships between exercise, mitochondrial proteostasis, and PD and explore the role and mechanisms of mitochondrial proteostasis in delaying PD through exercise.

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Treadmill exercise attenuates cerebral ischaemic injury in rats by protecting mitochondrial function via enhancement of caveolin-1

Cited by 9 publications

References 44 publications

Synapsin-Promoted Caveolin-1 Overexpression Maintains Mitochondrial Morphology and Function in PSAPP Alzheimer’s Disease Mice

Synapsin-Promoted Caveolin-1 Overexpression Maintains Mitochondrial Morphology and Function in PSAPP Alzheimer’s Disease Mice

Exercise sustains the hallmarks of health

The Role of Exercise in Maintaining Mitochondrial Proteostasis in Parkinson’s Disease

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