Redox Regulation of Mitochondrial Potassium Channels Activity

Lewandowska, Joanna; Kalenik, Barbara; Wrzosek, Antoni; Szewczyk, Adam

doi:10.3390/antiox13040434

Cited by 2 publications

(2 citation statements)

References 145 publications

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“…Additionally, mitochondrial tandem pore domain K + channels TASK-3 interact also with the respiratory chain. A recent report revealed a similar interaction between the mitoKv1.3 channel and respiratory chain complex I (for review see Lewandowska et al, 2024).…”

Section: Mitochondrial Context Of Potassium Channel Regulationmentioning

confidence: 95%

“…It is well-known that mitoK channels interact with various mitochondrial proteins, some of which are involved in the respiratory chain. These observations were recently summarized (Lewandowska et al, 2024). For instance, it has been suggested that mitoK ATP channels interact with succinate dehydrogenase.…”

Section: Mitochondrial Context Of Potassium Channel Regulationmentioning

confidence: 99%

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Understanding mitochondrial potassium channels: 33 years after discovery

Szewczyk

2024

Acta Biochim. Pol.

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Mitochondrial investigations have extended beyond their traditional functions, covering areas such as ATP synthesis and metabolism. Mitochondria are now implicated in new functional areas such as cytoprotection, cellular senescence, tumor function and inflammation. The basis of these new areas still relies on fundamental biochemical/biophysical mitochondrial functions such as synthesis of reactive oxygen species, mitochondrial membrane potential, and the integrity of the inner mitochondrial membrane i.e., the passage of various molecules through the mitochondrial membranes. In this view transport of potassium cations, known as the potassium cycle, plays an important role. It is believed that K+ influx is mediated by various potassium channels present in the inner mitochondrial membrane. In this article, we present an overview of the key findings and characteristics of mitochondrial potassium channels derived from research of many groups conducted over the past 33 years. We propose a list of six fundamental observations and most important ideas dealing with mitochondrial potassium channels. We also discuss the contemporary challenges and future prospects associated with research on mitochondrial potassium channels.

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Section: Mitochondrial Context Of Potassium Channel Regulationmentioning

confidence: 95%

Section: Mitochondrial Context Of Potassium Channel Regulationmentioning

confidence: 99%

Understanding mitochondrial potassium channels: 33 years after discovery

Szewczyk

2024

Acta Biochim. Pol.

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Borna disease virus 1 induces ferroptosis, contributing to lethal encephalitis

Tan,

Yang,

et al. 2024

Journal of Medical Virology

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Borna disease virus 1 (BoDV‐1) is a neurotropic RNA virus that has been linked to fatal BoDV‐1 encephalitis (BVE) in humans. Ferroptosis represents a newly recognized kind of programmed cell death that marked by iron overload and lipid peroxidation. Various viral infections are closely related to ferroptosis. However, the link between BoDV‐1 infection and ferroptosis, as well as its role in BVE pathogenesis, remains inadequately understood. Herein, we used primary rat cortical neurons, human microglial HMC3 cells, and Sprague‒Dawley rats as models. BoDV‐1 infection induced ferroptosis, as ferroptosis characteristics were detected (iron overload, reactive oxygen species buildup, decreased antioxidant capacity, lipid peroxidation, and mitochondrial damage). Analysis via qRT‐PCR and Western blot demonstrated that BoDV‐1‐induced ferroptosis was mediated through Nrf2/HO‐1/SLC7a11/GPX4 antioxidant pathway suppression. Nrf2 downregulation was due to BoDV‐1 infection promoting Nrf2 ubiquitination and degradation. Following BoDV‐1‐induced ferroptosis, the PTGS2/PGE2 signaling pathway was activated, and various intracellular lipid peroxidation products and damage‐associated molecular patterns were released, contributing to BVE occurrence and progression. More importantly, inhibiting ferroptosis or the ubiquitin‒proteasome system effectively alleviated BVE. Collectively, these findings demonstrate the interaction between BoDV‐1 infection and ferroptosis and reveal BoDV‐1‐induced ferroptosis as an underlying pathogenic mechanism of BVE.

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Redox Regulation of Mitochondrial Potassium Channels Activity

Cited by 2 publications

References 145 publications

Understanding mitochondrial potassium channels: 33 years after discovery

Understanding mitochondrial potassium channels: 33 years after discovery

Borna disease virus 1 induces ferroptosis, contributing to lethal encephalitis

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