Ionic signalling and mitochondrial dynamics

Abuarab, Nada; Li, Fangfang; Sivaprasadarao, Asipu

doi:10.1080/23723556.2017.1373889

Cited by 3 publications

(4 citation statements)

References 10 publications

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“…Zinc causes mitochondrial morphology changes such as mitochondrial fragmentation, evidenced by the formation of small, round mitochondrial puncta [ 238 , 239 , 240 , 241 ]. Zinc impairment of fusion–fission dynamics likely plays an important role in causing these morphological changes, as mitochondrial fragmentation and elongation are caused by excess fission and fusion, respectively [ 217 , 219 ].…”

Section: Zinc and Mitochondrial Dynamicsmentioning

confidence: 99%

“…Zinc impairment of fusion–fission dynamics likely plays an important role in causing these morphological changes, as mitochondrial fragmentation and elongation are caused by excess fission and fusion, respectively [ 217 , 219 ]. Activation of DRP1, which plays a critical role in fission [ 242 ], has been shown to contribute to mitochondrial fragmentation, and recent studies have demonstrated that zinc causes mitochondrial fragmentation via DRP1 activation in ß cells [ 239 , 240 , 243 ]. Moreover, zinc induces DRP1-mediated fission, resulting in mitochondrial fragmentation and mitochondrial network disruption in brain endothelial cells [ 241 ].…”

Section: Zinc and Mitochondrial Dynamicsmentioning

confidence: 99%

See 1 more Smart Citation

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Biomedicines

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Zinc is a highly abundant cation in the brain, essential for cellular functions, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. An increasing body of work suggests that intracellular zinc can, under certain circumstances, contribute to neuronal damage by inhibiting mitochondrial energy processes, including dissipation of the mitochondrial membrane potential (MMP), leading to ATP depletion. Additional consequences of zinc-mediated mitochondrial damage include reactive oxygen species (ROS) generation, mitochondrial permeability transition, and excitotoxic calcium deregulation. Zinc can also induce mitochondrial fission, resulting in mitochondrial fragmentation, as well as inhibition of mitochondrial motility. Here, we review the known mechanisms responsible for the deleterious actions of zinc on the organelle, within the context of neuronal injury associated with neurodegenerative processes. Elucidating the critical contributions of zinc-induced mitochondrial defects to neurotoxicity and neurodegeneration may provide insight into novel therapeutic targets in the clinical setting.

show abstract

Section: Zinc and Mitochondrial Dynamicsmentioning

confidence: 99%

Section: Zinc and Mitochondrial Dynamicsmentioning

confidence: 99%

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Biomedicines

View full text Add to dashboard Cite

show abstract

“…Zinc causes mitochondrial morphology changes such as mitochondrial fragmentation, evidenced by the formation of small, round mitochondrial puncta [233][234][235][236]. Zinc impairment of fusion-fission dynamics likely play an important role in causing these morphological changes, as mitochondrial fragmentation and elongation are caused by excess fission and fusion, respectively [212,214].…”

Section: Fission Fusion and Morphologymentioning

confidence: 99%

“…Zinc impairment of fusion-fission dynamics likely play an important role in causing these morphological changes, as mitochondrial fragmentation and elongation are caused by excess fission and fusion, respectively [212,214]. In fact, activation of DRP1, which plays a critical role in fission [237], has been shown to contribute to mitochondrial fragmentation, and recent studies have demonstrated that zinc causes mitochondrial fragmentation via DRP1 activation in ß cells [234,235,238]. Moreover, zinc induces DRP1-mediated fission, resulting in mitochondrial fragmentation and mitochondrial network disruption in brain endothelial cells [236].…”

Section: Fission Fusion and Morphologymentioning

confidence: 99%

The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction

Liu

Gale

Reynolds³

et al. 2021

Preprint

View full text Add to dashboard Cite

Zinc is a highly abundant cation in the brain, where it is essential for cellular function, including transcription, enzymatic activity, and cell signaling. However, zinc can also trigger injurious cascades in neurons, contributing to the pathology of neurodegenerative diseases. Mitochondria, critical for meeting the high energy demands of the central nervous system (CNS), are a principal target of the deleterious actions of zinc. An increasing body of work suggests that intracellular zinc, can, under certain circumstances, contribute to neuronal damage by inhibiting mitochondrial energy processes, including dissipation of the mitochondrial membrane potential, leading to ATP depletion. Additional consequences of zinc-mediated mitochondrial damage include reactive oxygen species (ROS) generation, mitochondrial permeability transition, and calcium deregulation. Zinc can also induce mitochondrial fission, resulting in mitochondrial fragmentation, as well as inhibition of mitochondrial motility. Here, we review the known mechanisms responsible for the deleterious actions of zinc on the organelle, within the context of neuronal injury associated with neurodegenerative processes. Elucidating the critical contributions of zinc-induced mitochondrial defects to neurotoxicity and neurodegeneration may provide insight into novel therapeutic targets in the clinical setting.

show abstract