Loss of Kir6.1 facilitates peri-infarct depolarizations in focal cerebral ischemia

Zheng, Zijie; Li, Zhenyu; Liu, Jianping

doi:10.1080/01616412.2022.2051132

Cited by 3 publications

(2 citation statements)

References 35 publications

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“…Also, activation of K ATP channels has a protective effect in ischemic postconditioning, not only in the cardiac system, but also in the central nervous system. Indeed, in vivo animal studies demonstrated that knocking out Kir6.2 exacerbates ischemic infarction, while overexpressing Kir6.2 ameliorates neuronal injury from ischemic insults (Morisaki et al, 2022;Pertiwi et al, 2019;Zhao et al, 2021b;Zheng et al, 2022).…”

Section: K Atp Is Involved In Neuronal Protection and Selective Vulne...mentioning

confidence: 99%

Potassium Channels in Parkinson’s Disease: Potential Roles in Its Pathogenesis and Innovative Molecular Targets for Treatment

et al. 2023

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A-type voltage-dependent K + currents IC 50 Half maximal inhibitory concentration IK Intermediate-conductance calcium-activated potassium (channel) iNOS Inducible nitric oxide synthase K 2 P Two-pore-domain potassium (channel) K ATP ATP-sensitive potassium (channel) K Ca Calcium-activated potassium (channel) Kir Inwardly rectifying potassium (channel) K V Voltage-gated potassium (channel) LTCC L-type voltage-gated calcium channel MgTx Margatoxin mito-K ATP Mitochondrial ATP-sensitive potassium (channel) mTOR Mammalian target of rapamycin Na V Voltage-gated sodium (channel) NMDAR N-methyl-D-aspartate receptor NO Nitric oxide PD Parkinson's disease PGC Peroxisome proliferator-activated receptor-gamma coactivator PIP 2 Phosphatidylinositol 4,5-bisphosphate PKA Protein kinase A PM Plasma membrane has not been copyedited and formatted. The final version may differ from this version.

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Section: K Atp Is Involved In Neuronal Protection and Selective Vulne...mentioning

confidence: 99%

Potassium Channels in Parkinson’s Disease: Potential Roles in Its Pathogenesis and Innovative Molecular Targets for Treatment

et al. 2023

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“…When ATP drops, K ATP channels open, hyperpolarizing the neuron and decreasing the probability of firing. Zheng et al evaluated K ATP knock‐out mice during experimental focal ischemic stroke, and reported that K ATP disruption increased susceptibility to peri‐infarct SDs (Zheng et al, 2022). Similarly, pharmacological activation or inhibition of K ATP in a locust model delayed or accelerated (respectively) the onset of SD induced by anoxia (Van Dusen et al, 2020).…”

Section: Metabolic Burden Of Sdmentioning

confidence: 99%

Spreading depolarizations pose critical energy challenges in acute brain injury

Lindquist

2023

Journal of Neurochemistry

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Spreading depolarization (SD) is an electrochemical wave of neuronal depolarization mediated by extracellular K+ and glutamate, interacting with voltage‐gated and ligand‐gated ion channels. SD is increasingly recognized as a major cause of injury progression in stroke and brain trauma, where the mechanisms of SD‐induced neuronal injury are intimately linked to energetic status and metabolic impairment. Here, I review the established working model of SD initiation and propagation. Then, I summarize the historical and recent evidence for the metabolic impact of SD, transitioning from a descriptive to a mechanistic working model of metabolic signaling and its potential to promote neuronal survival and resilience. I quantify the energetic cost of restoring ionic gradients eroded during SD, and the extent to which ion pumping impacts high‐energy phosphate pools and the energy charge of affected tissue. I link energy deficits to adaptive increases in the utilization of glucose and O2, and the resulting accumulation of lactic acid and CO2 downstream of catabolic metabolic activity. Finally, I discuss the neuromodulatory and vasoactive paracrine signaling mediated by adenosine and acidosis, highlighting these metabolites' potential to protect vulnerable tissue in the context of high‐frequency SD clusters.image

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CRISPR-Cas9 homology-independent targeted integration of exons 1–19 restores full-length dystrophin in mice

Stephenson,

Nicolau,

Vetter

et al. 2023

Molecular Therapy - Methods & Clinical Development

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Loss of Kir6.1 facilitates peri-infarct depolarizations in focal cerebral ischemia

Cited by 3 publications

References 35 publications

Potassium Channels in Parkinson’s Disease: Potential Roles in Its Pathogenesis and Innovative Molecular Targets for Treatment

Potassium Channels in Parkinson’s Disease: Potential Roles in Its Pathogenesis and Innovative Molecular Targets for Treatment

Spreading depolarizations pose critical energy challenges in acute brain injury

CRISPR-Cas9 homology-independent targeted integration of exons 1–19 restores full-length dystrophin in mice

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