Exercise induces mitochondrial biogenesis after brain ischemia in rats

Zhang, Q.; Wu, Yi; Zhang, P.; Sha, Hao; Jia, Jie; Hu, Ya-Han; Zhu, Jiaan

doi:10.1016/j.neuroscience.2011.12.053

Cited by 105 publications

(53 citation statements)

References 30 publications

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“…Previous reports [52][53][54] have suggested that exercise training promotes mitochondria biogenesis by increasing mitochondrial number, content, volume and function. Hence, we can postulate that exercise training may ameliorate the oxidative environment caused by the mitochondrial abnormalities in the PD skeletal muscles.…”

Section: Discussionmentioning

confidence: 93%

Endurance Exercise Training Attenuates the up Regulation of iNOS in the Skeletal Muscles of Chronic/Progressive Mouse Model of Parkinson’s Disease

Erekat

2013

J Neurol Res

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Background: Parkinson's disease (PD) is one of the most common neurodegenerative diseases in the elderly. PD complications include muscle weakness and fatigue, these complications lead in part to decrease the endurance of PD patients. Strength of skeletal muscles has a major role in ADL performance, which is one of the challenges that PD patients have. The main goals of this study are to study the expression of inducible nitric oxide synthase (iNOS) in the skeletal muscles of PD and to examine the effect of treadmill exercise training on iNOS expression in these skeletal muscles.

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Section: Discussionmentioning

confidence: 93%

Endurance Exercise Training Attenuates the up Regulation of iNOS in the Skeletal Muscles of Chronic/Progressive Mouse Model of Parkinson’s Disease

Erekat

2013

J Neurol Res

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“…However, it is believed that the beginning of the exercise program may have been too late (fourth postoperative day). Some studies that started the exercise program 1 day after cerebral ischemia showed recovery in the region of cerebral ischemia (Liu et al, 2011;Zhang et al, 2012a;2012b).…”

Section: Discussionmentioning

confidence: 99%

“…The exercises after MCAO (DI) and after the sham operation (DC) lasted 6 weeks and the rats exercised for 30 min/day, on the treadmill without inclination, 5 days per week, with a speed of 12 m/min (Liu et al, 2011;Zhang et al 2012a;2012b). The exercise speed was gradually increased: On the first day the rats ran with a speed 8 m/min, on the second day at 10 m/min and on the third day at 12 m/min (Liu et al, 2011;Zhang et al 2012a;2012b).…”

Section: Physical Trainingmentioning

confidence: 99%

“…The exercise speed was gradually increased: On the first day the rats ran with a speed 8 m/min, on the second day at 10 m/min and on the third day at 12 m/min (Liu et al, 2011;Zhang et al 2012a;2012b). The rats that were able to run for 2 min at speeds of 8, 11 and 12 m/min in the first 3 days of the physical training continued in the research.…”

Section: Physical Trainingmentioning

confidence: 99%

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Effect of Exercise Prior or After Ischemia on the Density of Neurons and Astrocytes in the Brain of Rats

Damázio¹,

Melo²,

Lima³

et al. 2014

American Journal of Neuroscience

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The aim of this study was to analyse the density of astrocytes and neurons in the motor areas of the cortex, striatum and hippocampus of rats that performed exercise before or after cerebral ischemia. A total of 36 Wistar rats were separated into two groups: One that was subjected to Middle Cerebral Artery Occlusion (MCAO) and the other that underwent surgical access in the absence of ischemia. Both groups were subdivided into: Animals that underwent exercise prior to MCAO and sham surgery (AI and AC, n = 12); animals that underwent exercise after MCAO and sham surgery (DI and DC, n = 12); and animals that did not undergo exercise (SI and SC, n = 12). The brains of mice were sectioned and stained by the Nissl method for staining of neurons and the astrocytes were labeled by immunohistochemistry with glial fibrillary acidic protein. Physical training was conducted after the surgery for 6 weeks (30 min/day), 5 days per week. The animals exercised before cerebral ischemia showed greater density of neurons in the striatum, in the apex of the dentate gyrus of the hippocampus, in the motor cortex contra lateral to the lesion and more astrocytes in the motor cortex of the cerebral hemispheres compared with the untrained group (p<0.05). The density of neurons in the brain regions analysed remained unchanged in exercised animals from the fourth day after cerebral ischemia when compared with the sedentary group.

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“…Exercise is a well-known activator of mitochondrial biogenesis by upregulating PGC-1α [116]. In addition to its effects on skeletal muscle, exercise training was shown to increase mitochondrial biogenesis in the brain [117], highlighting exercise as a complementary strategy for neuroprotection and management of mitochondrial-associated neurological disease [118].…”

Section: Biogenesis and Fission-fusionmentioning

confidence: 99%

Trends in Mitochondrial Therapeutics for Neurological Disease

Leitão-Rocha¹,

Guedes-Dias²,

Pinho³

et al. 2015

CMC

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Neuronal homeostasis is critically dependent on healthy mitochondria. Mutations in mitochondrial DNA (mtDNA), in nuclear-encoded mitochondrial components, and agedependent mitochondrial damage, have all been connected with neurological disorders. These include not only typical mitochondrial syndromes with neurological features such as encephalomyopathy, myoclonic epilepsy, neuropathy and ataxia; but also secondary mitochondrial involvement in neurodegenerative disorders such as Alzheimer's, Parkinson's and Huntington's disease. Unravelling the molecular aetiology of mitochondrial dysfunction opens new therapeutic prospects for diseases thus far lacking effective treatments. In this review we address recent advances on preventive strategies, such as pronuclear, spindlechromosome complex, or polar body genome transfer to replace mtDNA and avoid disease transmission to newborns; we also address experimental mitochondrial therapeutics aiming to benefit symptomatic patients and prevent disease manifestation in those at risk. Specifically, we focus on: (1) gene therapy to reduce mutant mtDNA, such as anti-replicative therapies and mitochondria-targeted nucleases allowing favourable heteroplasmic shifts; (2) allotopic expression of recoded wild-type mitochondrial genes, including targeted tRNAs and xenotopic expression of cognate genes to compensate for pathogenic mutations; (3) mitochondria targeted-peptides and lipophilic cations for in vivo delivery of antioxidants or other putative therapeutics; and (4) modulation of mitochondrial dynamics at the level of biogenesis, fission, fusion, movement and mitophagy. Further advances in therapeutic development are hindered by scarce in vivo models for mitochondrial disease, with the bulk of available data coming from cellular models. Nevertheless, wherever available, we also address data from in vivo experiments and clinical trials, focusing on neurological disease models.

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Exercise induces mitochondrial biogenesis after brain ischemia in rats

Cited by 105 publications

References 30 publications

Endurance Exercise Training Attenuates the up Regulation of iNOS in the Skeletal Muscles of Chronic/Progressive Mouse Model of Parkinson’s Disease

Endurance Exercise Training Attenuates the up Regulation of iNOS in the Skeletal Muscles of Chronic/Progressive Mouse Model of Parkinson’s Disease

Effect of Exercise Prior or After Ischemia on the Density of Neurons and Astrocytes in the Brain of Rats

Trends in Mitochondrial Therapeutics for Neurological Disease

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