Ischemic stroke and mitochondria: mechanisms and targets

Andrabi, Syed Suhail; Parvez, Suhel; Tabassum, Heena

doi:10.1007/s00709-019-01439-2

Cited by 127 publications

(88 citation statements)

References 77 publications

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“…And that make further efforts to increase the expression of ROS in a feed forward manner [35,36]. In this way, that kind of loop promotes the accumulation of ROS, leading to mitochondrial damage and activation of mitochondrial-mediated apoptosis [37]. When we studied the expression of ROS in microglia and the change of mitochondrial membrane potential, we found that rhTrx-1 effectively inhibited the pathological accumulation of ROS and rescued mitochondrial injury.…”

Section: Discussionmentioning

confidence: 94%

RhTrx-1 ameliorates miroglial neuroinflammation after cerebral ischemic stroke

Jiao¹,

Wang²,

Zhang³

et al. 2020

Preprint

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Background Microglia are rapidly activated after ischemic stroke and participate in the occurrence of neuroinflammation, which exacerbates the injury of ischemic stroke. Receptor Interacting Serine Threonine Kinase 1 (RIPK1) is thought to be involved in the development of inflammatory responses, but its role in ischemic microglia remains unclear. Here, we applied recombinant human thioredoxin-1 (rhTrx-1), a potential neuroprotective agent, to explore the role of rhTrx-1 in inhibiting RIPK1-mediated neuroinflammatory responses in microglia. Method Middle cerebral artery occlusion (MCAO) and Oxygen and glucose deprivation (OGD) were conducted for in vivo and in vitro experimental stroke models. The expression of RIPK1 in microglia after ischemia was examined. The inflammatory response of microglia was analyzed after treatment with rhTrx-1 and Necrostatin-1 (Nec-1, inhibitors of RIPK1), and the mechanisms were explored. In addition, the effects of rhTrx-1 on neurobehavioral deficits and cerebral infarct volume were examined. Results RIPK1 expression was detected in microglia after ischemia. Molecular docking results showed that rhTrx-1 could directly bind to RIPK1. In vitro experiments found that rhTrx-1 reduced necroptosis, mitochondrial membrane potential damage, Reactive oxygen species (ROS) accumulation and NLR Family, pyrin domain-containing 3 protein (NLRP3) inflammasome activation by inhibiting RIPK-1 expression, and regulated microglial M1/M2 phenotypic changes, thereby reducing the release of inflammatory factors. Consistently, in vivo experiments found that rhTrx-1 treatment attenuated cerebral ischemic injury by inhibiting the inflammatory response. Conclusion Our study demonstrates the role of RIPK1 in microglia-arranged neuroinflammation after cerebral ischemia. Administration of rhTrx-1 provides neuroprotection in ischemic stroke-induced microglial neuroinflammation by inhibiting RIPK1 expression.

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Section: Discussionmentioning

confidence: 94%

RhTrx-1 ameliorates miroglial neuroinflammation after cerebral ischemic stroke

Jiao¹,

Wang²,

Zhang³

et al. 2020

Preprint

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“…And that make further efforts to increase the production of ROS in a feed forward manner 37,38 . In this way, the feedback loop promotes the accumulation of ROS, leading to mitochondrial damage and activation of mitochondrial‐mediated caspase‐3 activation 39 . To figure out, in the present study, the production of ROS in microglia and the change in the mitochondrial membrane potential were examined and the data demonstrated that rhTrx‐1 and Nec‐1 effectively inhibited the pathological accumulation of ROS and rescued mitochondrial injury.…”

Section: Discussionmentioning

confidence: 99%

“…37,38 In this way, the feedback loop promotes the accumulation of ROS, leading to mitochondrial damage and activation of mitochondrial-mediated caspase-3 activation. 39 and by promoting the release of ROS, which further promotes the production and secretion of IL-1β to the extracellular space and initiates neuroinflammation. Furthermore, the activation of RIPK3-MLKL can directly trigger the activation of the NLRP3 inflammasome.…”

Section: F I G U R Ementioning

confidence: 99%

Inhibition of microglial receptor‐interacting protein kinase 1 ameliorates neuroinflammation following cerebral ischaemic stroke

Jiao

Wang

Zhang

et al. 2020

J Cellular Molecular Medi

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Section: Cerebral Ischemiamentioning

confidence: 99%

“…Radicals can induce the disruption of the inner mitochondrial membrane and further negatively affect ATP production. Moreover, damaged mitochondria release pro-apoptotic signals, leading to cell death [ 136 ]. Ischemic damage and processes occurring thereafter lead to neuroinflammation, in which glial cells, particularly microglia, but also astrocytes, are involved [ 137 ].…”

Section: Cerebral Ischemiamentioning

confidence: 99%

Glia and Neural Stem and Progenitor Cells of the Healthy and Ischemic Brain: The Workplace for the Wnt Signaling Pathway

Knotek

Janečková

Kriška

et al. 2020

Genes

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Wnt signaling plays an important role in the self-renewal, fate-commitment and survival of the neural stem/progenitor cells (NS/PCs) of the adult central nervous system (CNS). Ischemic stroke impairs the proper functioning of the CNS and, therefore, active Wnt signaling may prevent, ameliorate, or even reverse the negative effects of ischemic brain injury. In this review, we provide the current knowledge of Wnt signaling in the adult CNS, its status in diverse cell types, and the Wnt pathway’s impact on the properties of NS/PCs and glial cells in the context of ischemic injury. Finally, we summarize promising strategies that might be considered for stroke therapy, and we outline possible future directions of the field.

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Ischemic stroke and mitochondria: mechanisms and targets

Cited by 127 publications

References 77 publications

RhTrx-1 ameliorates miroglial neuroinflammation after cerebral ischemic stroke

RhTrx-1 ameliorates miroglial neuroinflammation after cerebral ischemic stroke

Inhibition of microglial receptor‐interacting protein kinase 1 ameliorates neuroinflammation following cerebral ischaemic stroke

Glia and Neural Stem and Progenitor Cells of the Healthy and Ischemic Brain: The Workplace for the Wnt Signaling Pathway

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