Scutellarin ameliorates high glucose-induced vascular endothelial cells injury by activating PINK1/Parkin-mediated mitophagy

Xi, Junxiao; Rong, Yuezhao; Zhao, Zifeng; Huang, Yao; Wang, Pu; Luan, Huiling; Xing, Yan; Liu, Siyuan; Liao, Jun; Dai, Yue; Liang, Jing‐Yu; Wu, Feihua

doi:10.1016/j.jep.2021.113855

Cited by 52 publications

(34 citation statements)

References 43 publications

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“…However, the effect is weakened by PINK1 gene knockdown. These results remind that scutellarin suppresses vascular endothelial cell damage caused by hyperglycemia through activating PINK1/Parkin-dependent mitophagy (Table 2 and Figure 3; Xi et al, 2021).…”

Section: Liu Et Al 2018supporting

confidence: 64%

Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders

Guo

Huang

et al. 2021

Front. Cell Dev. Biol.

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Metabolic disorders include metabolic syndrome, obesity, type 2 diabetes mellitus, non-alcoholic fatty liver disease and cardiovascular diseases. Due to unhealthy lifestyles such as high-calorie diet, sedentary and physical inactivity, the prevalence of metabolic disorders poses a huge challenge to global human health, which is the leading cause of global human death. Mitochondrion is the major site of adenosine triphosphate synthesis, fatty acid β−oxidation and ROS production. Accumulating evidence suggests that mitochondrial dysfunction-related oxidative stress and inflammation is involved in the development of metabolic disorders. Mitophagy, a catabolic process, selectively degrades damaged or superfluous mitochondria to reverse mitochondrial dysfunction and preserve mitochondrial function. It is considered to be one of the major mechanisms responsible for mitochondrial quality control. Growing evidence shows that mitophagy can prevent and treat metabolic disorders through suppressing mitochondrial dysfunction-induced oxidative stress and inflammation. In the past decade, in order to expand the range of pharmaceutical options, more and more phytochemicals have been proven to have therapeutic effects on metabolic disorders. Many of these phytochemicals have been proved to activate mitophagy to ameliorate metabolic disorders. Given the ongoing epidemic of metabolic disorders, it is of great significance to explore the contribution and underlying mechanisms of mitophagy in metabolic disorders, and to understand the effects and molecular mechanisms of phytochemicals on the treatment of metabolic disorders. Here, we investigate the mechanism of mitochondrial dysfunction in metabolic disorders and discuss the potential of targeting mitophagy with phytochemicals for the treatment of metabolic disorders, with a view to providing a direction for finding phytochemicals that target mitophagy to prevent or treat metabolic disorders.

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Section: Liu Et Al 2018supporting

confidence: 64%

Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders

Guo

Huang

et al. 2021

Front. Cell Dev. Biol.

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“…Scutellarin ameliorated high glucose-induced vascular endothelial cells injury by activating PINK1/Parkin signal pathway-mediated mitophagy. It improved the overload of ROS, superoxide dismutase (SOD) activity and SOD2 protein expression, and reversed the collapse of MMP in high glucoseinduced vascular endothelial cells model (Xi et al, 2021). Scutellarin may have a similar mechanism as edaravone.…”

Section: Discussionmentioning

confidence: 99%

Dengzhanxixin Injection Ameliorates Cognitive Impairment Through a Neuroprotective Mechanism Based on Mitochondrial Preservation in Patients With Acute Ischemic Stroke

Wan

Liang

et al. 2021

Front. Pharmacol.

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Acute ischemic stroke (AIS) is a global health burden and cognitive impairment is one of its most serious complication. Adequate interventions for AIS may have the potential to improve cognitive outcomes. In the present study, we selected Erigeron breviscapus (Vaniot) Hand.-Mazz. injection (Dengzhanxixin injection, DZXI), a widely used Chinese herbal injection, in contrast to edaravone as the positive control drug to test its potential to ameliorates neurological and cognitive impairments caused by AIS. We performed a 2-week randomized trial with these two drugs in AIS patients presenting mild to moderate cognitive impairments. Neuropsychological tests and MRI examinations showed that DZXI attenuated the neurological and cognitive impairments of patients and protected the grey matter in specific regions from ischemic damage. Notably, DZXI exerted better effects than edaravone in some neuropsychological tests, probably due to the protective effect of DZXI on grey matter. To explore the therapeutic mechanisms, we carried out an experiment with a middle cerebral artery occlusion rat model. We found that DZXI decreased the infarct volume and increased the survival of neuronal cells in the ischemic penumbra; furthermore, DZXI modulated the mitochondrial respiratory chain process and preserved the mitochondrial structure in the brain tissue. Overall, our data suggested that the administration of DZXI is effective at ameliorating neurological and cognitive impairments in AIS, and the underlying mechanisms are related to the protective effects of DZXI on cerebral neurons and neuronal mitochondria.

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“…PINK1 accumulation in the mitochondria activates PARKIN's E3 ubiquitin ligase activity and recruits PARKIN into the impaired mitochondria. This triggers the selective autophagic clearance of damaged mitochondria (Lazarou et al, 2012; Xi et al, 2021). Mutations in PINK1, PARKIN, DJ-1 and LRRK2 are linked to PD (Puspita et al, 2017).…”

Section: Mitochondrial Dysfunction In Pdmentioning

confidence: 99%

Mitochondrial and Organellar Crosstalk in Parkinson’s Disease

et al. 2021

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Mitochondrial dysfunction is a well-established pathological event in Parkinson’s disease (PD). Proteins misfolding and its impaired cellular clearance due to altered autophagy/mitophagy/pexophagy contribute to PD progression. It has been shown that mitochondria have contact sites with endoplasmic reticulum (ER), peroxisomes and lysosomes that are involved in regulating various physiological processes. In pathological conditions, the crosstalk at the contact sites initiates alterations in intracellular vesicular transport, calcium homeostasis and causes activation of proteases, protein misfolding and impairment of autophagy. Apart from the well-reported molecular changes like mitochondrial dysfunction, impaired autophagy/mitophagy and oxidative stress in PD, here we have summarized the recent scientific reports to provide the mechanistic insights on the altered communications between ER, peroxisomes, and lysosomes at mitochondrial contact sites. Furthermore, the manuscript elaborates on the contributions of mitochondrial contact sites and organelles dysfunction to the pathogenesis of PD and suggests potential therapeutic targets.

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Scutellarin ameliorates high glucose-induced vascular endothelial cells injury by activating PINK1/Parkin-mediated mitophagy

Cited by 52 publications

References 43 publications

Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders

Phytochemicals: Targeting Mitophagy to Treat Metabolic Disorders

Dengzhanxixin Injection Ameliorates Cognitive Impairment Through a Neuroprotective Mechanism Based on Mitochondrial Preservation in Patients With Acute Ischemic Stroke

Mitochondrial and Organellar Crosstalk in Parkinson’s Disease

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