The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing thePGC-1α–NRF1/NRF2Pathway and Mitochondrial Respiratory Function in Rats

Zheng, Ping; Zhang, Longfei; Cui, Yujuan; Chang, Yu‐Mei; Jiang, Cai-Wu; Meng, Ziqi; Xu, Peng; Liu, Haiyan; Wang, Dongying; Cao, Xuebin

doi:10.1155/2015/876825

Cited by 62 publications

(31 citation statements)

References 18 publications

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“…Nrf2 is moreover a downstream transcription factor for PGC-1α (peroxisome proliferatoractivated receptor gamma coactivator-1 alpha) gene. The Nrf2 and PGC-1α proteins interact with each other as well (the latter as co-factor) activating mitochondria-related genes, mentioned earlier in this chapter [142][143].…”

Section: The Pgc-1α-nrf2 Axis 21mentioning

confidence: 78%

Mitochondrial quality control in AMD: does mitophagy play a pivotal role?

Hyttinen

Viiri

Kaarniranta

et al. 2018

Cell. Mol. Life Sci.

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Age-related macular degeneration (AMD) is the predominant cause of visual loss in old people in the developed world, whose incidence is increasing. This disease is caused by the decrease in macular function, due to the degeneration of retinal pigment epithelium (RPE) cells. The aged retina is characterised by increased levels of reactive oxygen species (ROS), impaired autophagy, and DNA damage that are linked to AMD pathogenesis. Mitophagy, a mitochondria-specific type of autophagy, is an essential part of mitochondrial quality control, the collective mechanism responsible for this organelle's homeostasis. The abundance of ROS, DNA damage, and the excessive energy consumption in the ageing retina all contribute to the degeneration of RPE cells and their mitochondria. We discuss the role of mitophagy in the cell and argue that its impairment may play a role in AMD pathogenesis. Thus, mitophagy as a potential therapeutic target in AMD and other degenerative diseases is as well explored.

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Section: The Pgc-1α-nrf2 Axis 21mentioning

confidence: 78%

Mitochondrial quality control in AMD: does mitophagy play a pivotal role?

Hyttinen

Viiri

Kaarniranta

et al. 2018

Cell. Mol. Life Sci.

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“…RS is a member of the Rhodiola family that is grown in Tibet in China [ 27 ]; this natural plant pharmaceutical is well known for its physiological benefits such as elimination of fatigue [ 43 ], enhancement of EC [ 28 ], and prolongation of lifespan [ 29 , 30 ]. Several recent studies have demonstrated that RS activates autophagy [ 44 ] and mitochondrial biogenesis in endothelial cells [ 33 ] and the myocardium in rats [ 45 ]. Here, we report for the first time that RS enhances the function of mitochondria in SCM and activates autophagy and mitochondrial biogenesis in mouse skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

Exercise Combined with Rhodiola sacra Supplementation Improves Exercise Capacity and Ameliorates Exhaustive Exercise‐Induced Muscle Damage through Enhancement of Mitochondrial Quality Control

Dun

Liu

Zhang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Mounting evidence has firmly established that increased exercise capacity (EC) is associated with considerable improvements in the survival of patients with cardiovascular disease (CVD) and that antistress capacity is a prognostic predictor of adverse cardiovascular events in patients with CVD. Previous studies have indicated that aerobic exercise (AE) and supplementation with Rhodiola sacra (RS), a natural plant pharmaceutical, improve EC and enable resistance to stress; however, the underlying mechanism remains unclear. This study explored the ability of AE and RS, alone or combined, to improve EC and ameliorate exhaustive exercise- (EE-) induced stress and elucidate the mechanism involved. We found that AE and RS significantly increased EC in mice and ameliorated EE-induced stress damage in skeletal and cardiac muscles (SCM); furthermore, a synergistic effect was detected for the first time. To our knowledge, the present work is the first to report that AE and RS activate mitophagy, mitochondrial dynamics, and biogenesis in SCM, both in the resting state and after EE. These data indicate that AE and RS synergistically improve EC in mice and protect SCM from EE-induced stress by enhancing mitochondrial quality control, including the activation of mitophagy, mitochondrial dynamics, and biogenesis, both at rest and after EE.

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“…Activation of the CREB pathway results in the phosphorylation of CREB (p-CREB), and p-CREB binds the CREB-response element (CRE), located proximal to the PGC-1α promoter, and activates PGC-1α transcription 42 , 43 . Additionally, GSK-3β plays a role in regulating PGC-1α protein stability, negatively regulating PGC-1α by promoting its proteasomal degradation 44 , 45 .…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effects of baicalein on rotenone-induced Parkinson’s disease through protecting mitochondrial function and biogenesis

Zhang

et al. 2017

Sci Rep

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Mitochondrial dysfunction has been implicated in the pathogenesis of Parkinson’s disease (PD) for several decades, and disturbed mitochondrial biogenesis (mitobiogenesis) was recently found to be a common phenomenon in PD. Baicalein, a major bioactive flavone of Scutellaria baicalensis Georgi, exerted neuroprotective effects in several experimental PD models. However, the effects of baicalein in rotenone-induced PD rats and the possible mechanisms remain poorly understood. In this study, we evaluated the therapeutic effects of baicalein and explored its mechanism of action in rotenone-induced PD models. The results indicated that behavioural impairments and the depletion of dopaminergic neurons induced by rotenone were attenuated by baicalein. Furthermore, in rotenone-induced parkinsonian rats, baicalein treatment effectively restored mitochondrial function and improved mitobiogenesis, as determined by measuring the mitochondrial density and key regulators involved in mitobiogenesis. Additionally, we confirmed that baicalein enhanced mitobiogenesis through the cAMP-responsive element binding protein (CREB) and glycogen synthase kinase-3β (GSK-3β) pathways in rotenone-treated SH-SY5Y cells. Moreover, we demonstrated that the cytoprotective effects of baicalein could be attenuated by the mitobiogenesis inhibitor chloramphenicol as well as CREB siRNA transfection. Overall, our results suggested that baicalein partially enhanced mitobiogenesis to restore mitochondrial function, thus exerting therapeutic effects in rotenone-induced PD models.

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The Protective Effects of Salidroside from Exhaustive Exercise-Induced Heart Injury by Enhancing thePGC-1α–NRF1/NRF2Pathway and Mitochondrial Respiratory Function in Rats

Cited by 62 publications

References 18 publications

Mitochondrial quality control in AMD: does mitophagy play a pivotal role?

Mitochondrial quality control in AMD: does mitophagy play a pivotal role?

Exercise Combined with Rhodiola sacra Supplementation Improves Exercise Capacity and Ameliorates Exhaustive Exercise‐Induced Muscle Damage through Enhancement of Mitochondrial Quality Control

Therapeutic effects of baicalein on rotenone-induced Parkinson’s disease through protecting mitochondrial function and biogenesis

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