Relationships Between Ion Channels, Mitochondrial Functions and Inflammation in Human Aging

Strickland, Marie; Yacoubi-Loueslati, Besma; Bouhaouala‐Zahar, Balkiss; Pender, Sylvia L.F.; Larbi, Anis

doi:10.3389/fphys.2019.00158

Cited by 52 publications

(45 citation statements)

References 308 publications

(312 reference statements)

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“…Anticonvulsants and antidepressants might aid in treating the pain of neuropathy [ 6 ]. More specifically, senolytic drugs (e.g., resveratrol) help to remove senescent cells to reduce the overall pro-inflammatory profile, although inflammation differs among tissues and makes it difficult to only target senescent cells [ 82 ]. Interestingly, resveratrol has been associated to promote mitochondrial health and renewal through different mechanisms [ 150 ].…”

Section: Treatment Strategies In Nmdsmentioning

confidence: 99%

“…Moreover, exercise has shown to induce autophagy to overcome sarcopenia (e.g., in metabolic myopathies) [ 152 ]. In young and old mice, exercise training has even promoted biogenesis of mitochondria and mitochondrial autophagy to reduce the expression of proinflammatory cytokines by up to 49% [ 82 ]. Unfortunately, exercise is not always possible in patients affected by NMDs.…”

Section: Treatment Strategies In Nmdsmentioning

confidence: 99%

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The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases

2020

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Neuromuscular diseases (NMDs) are a heterogeneous group of acquired or inherited rare disorders caused by injury or dysfunction of the anterior horn cells of the spinal cord (lower motor neurons), peripheral nerves, neuromuscular junctions, or skeletal muscles leading to muscle weakness and waste. Unfortunately, most of them entail serious or even fatal consequences. The prevalence rates among NMDs range between 1 and 10 per 100,000 population, but their rarity and diversity pose difficulties for healthcare and research. Some molecular hallmarks are being explored to elucidate the mechanisms triggering disease, to set the path for further advances. In fact, in the present review we outline the metabolic alterations of NMDs, mainly focusing on the role of mitochondria. The aim of the review is to discuss the mechanisms underlying energy production, oxidative stress generation, cell signaling, autophagy, and inflammation triggered or conditioned by the mitochondria. Briefly, increased levels of inflammation have been linked to reactive oxygen species (ROS) accumulation, which is key in mitochondrial genomic instability and mitochondrial respiratory chain (MRC) dysfunction. ROS burst, impaired autophagy, and increased inflammation are observed in many NMDs. Increasing knowledge of the etiology of NMDs will help to develop better diagnosis and treatments, eventually reducing the health and economic burden of NMDs for patients and healthcare systems.

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Section: Treatment Strategies In Nmdsmentioning

confidence: 99%

Section: Treatment Strategies In Nmdsmentioning

confidence: 99%

The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases

2020

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“…Osteoarthritis and rheumatoid arthritis Compromised mitochondrial respiration complex activities, ATP synthesis, ψ m and increased oxidative stress Johnson et al, 2000;Maneiro et al, 2003;Davies et al, 2008;Filippin et al, 2008;Liu et al, 2010;Biniecka et al, 2011;Lopez-Armada et al, 2013 Inflammaging Inflammasome activation, decreased mitochondrial respiration, increased glycolysis Franceschi et al, 2018;Strickland et al, 2019 Cardiovascular disorders and heart failure Increased oxidative stress, increased mitochondrial Ca 2+ , mtDNA mutations Maass et al, 2005;Garg, 2011;Oka et al, 2012;Lopez-Armada et al, 2013 Neurological disorders Oxidative stress leading to release of pro inflammatory cytokine Whitton, 2007;von Bernhardi and Eugenin, 2012;Lopez-Armada et al, 2013 Metabolic disorders (diabetes and obesity)…”

Section: Name Of the Disease Mitochondrial Defects Referencesmentioning

confidence: 99%

“…In addition to their response to injury or infection, inflammatory processes also facilitate 'inflammaging' (Salminen et al, 2012), a process where accelerated aging is mediated via changes in the redox-state of the cell. The role of mitochondria in inflammaging has been extensively discussed in a recent review (Strickland et al, 2019) and hence, will not be focused on here. In this review, we will describe and discuss the various mechanisms by which mitochondria determine the generation of inflammatory responses (section "Mitochondria and Inflammatory Response").…”

Section: Introductionmentioning

confidence: 99%

Insights Into the Role of Mitochondrial Ion Channels in Inflammatory Response

Ponnalagu

Singh

2020

Front. Physiol.

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Mitochondria are the source of many pro-inflammatory signals that cause the activation of the immune system and generate inflammatory responses. They are also potential targets of pro-inflammatory mediators, thus triggering a severe inflammatory response cycle. As mitochondria are a central hub for immune system activation, their dysfunction leads to many inflammatory disorders. Thus, strategies aiming at regulating mitochondrial dysfunction can be utilized as a therapeutic tool to cure inflammatory disorders. Two key factors that determine the structural and functional integrity of mitochondria are mitochondrial ion channels and transporters. They are not only important for maintaining the ionic homeostasis of the cell, but also play a role in regulating reactive oxygen species generation, ATP production, calcium homeostasis and apoptosis, which are common pro-inflammatory signals. The significance of the mitochondrial ion channels in inflammatory response is still not clearly understood and will need further investigation. In this article, we review the different mechanisms by which mitochondria can generate the inflammatory response as well as highlight how mitochondrial ion channels modulate these mechanisms and impact the inflammatory processes.

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“…VGCCs are known to play important roles in glioma biology such as cell proliferation, apoptosis, and sensitization to ionizing radiation 27,75,76 . VGCCs can be categorized as high voltage activated (HVA) or low voltage activated (LVA) types [77][78][79] . Among the HVA VGCCs, four subtypes can be categorized by electrophysiological property and genetic phylogeny, including L-type (long-lasting, Ca v 1.…”

Section: E Glioblastoma Electrotaxis Is Mediated By Voltage-gated Iomentioning

confidence: 99%

Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice

Tsai

IJspeert

Shen

2020

Preprint

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Transformed astrocytes in the most aggressive form cause glioblastoma, the most common cancer in central nervous system with high mortality. The physiological electric field by neuronal local field potentials and tissue polarity may guide the infiltration of glioblastoma cells through the electrotaxis process. However, microenvironments with multiplex gradients are difficult to create. In this work, we have developed a hybrid microfluidic platform to study glioblastoma electrotaxis in controlled microenvironments with high throughput quantitative analysis by a machine learning-powered single cell tracking software. By equalizing the hydrostatic pressure difference between inlets and outlets of the microchannel, uniform single cells can be seeded reliably inside the microdevice. The electrotaxis of two glioblastoma models, T98G and U-251MG, require optimal laminin-containing extracellular matrix and exhibits opposite directional and electro-alignment tendencies. Calcium signaling is a key contributor in glioblastoma pathophysiology but its role in glioblastoma electrotaxis is still an open question. Anodal T98G electrotaxis and cathodal U-251MG electrotaxis require the presence of extracellular calcium cations. U-251MG electrotaxis is dependent on the P/Q-type voltage-gated calcium channel (VGCC) and T98G is dependent on the R-type VGCC. U-251MG and T98G electrotaxis are also mediated by A-type (rapidly inactivating) voltage-gated potassium channels and acidsensing sodium channels. The involvement of multiple ion channels suggests that the glioblastoma electrotaxis is complex and patient-specific ion channel expression can be critical to develop personalized therapeutics to fight against cancer metastasis. The hybrid microfluidic design and machine learning-powered single cell analysis provide a simple and flexible platform for quantitative investigation of complicated biological systems.

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Relationships Between Ion Channels, Mitochondrial Functions and Inflammation in Human Aging

Cited by 52 publications

References 308 publications

The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases

The Impact of Mitochondrial Deficiencies in Neuromuscular Diseases

Insights Into the Role of Mitochondrial Ion Channels in Inflammatory Response

Voltage-gated ion channels mediate the electrotaxis of glioblastoma cells in a hybrid PMMA/PDMS microdevice

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