Mitochondria in Health and Disease – 3rd Annual Conference of Society for Mitochondrial Research and Medicine – 19–20 December 2013 — Bengaluru, India

Durhuus, Jon Ambæk; Desler, Claus; Rasmussen, Lene Juel

doi:10.1016/j.mito.2014.10.004

Cited by 5 publications

(5 citation statements)

References 29 publications

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“…Mitochondria, “powerhouse of cells”, play a vital role in energy metabolism and their dysfunction is tightly linked to the etiology and development of Parkinson’s disease, Alzheimer’s disease, diabetes and osteoporosis [33, 34]. Mitochondria can sense danger signals and exacerbate inflammation by controlling their function and activating the innate immune system [34].…”

Section: Discussionmentioning

confidence: 99%

“…Mitochondria can sense danger signals and exacerbate inflammation by controlling their function and activating the innate immune system [34]. Indeed, TNF-α down-regulated mitochondrial membrane potential and ATP production as compared to the vehicle-treated group, suggesting a role of perturbed mitochondrial function in this osteoblast inflammatory model.…”

Section: Discussionmentioning

confidence: 99%

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Drp1-dependent mitochondrial fission mediates osteogenic dysfunction in inflammation through elevated production of reactive oxygen species

Zhang¹,

Gan²,

He³

et al. 2017

PLoS ONE

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Although previous studies have implicated pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), to be detrimental for osteogenic activity, the related regulatory mechanisms are not yet fully validated. Since mitochondria host several essential metabolic processes and play a pivotal role in cellular functions, whether and how mitochondrial function contributes to inflammation-induced bone destruction needs further exploration. Our findings revealed that TNF-α impaired osteoblast function, including decreased mRNA levels of osteogenic markers, suppressed ALP expression and activity, and compromised cellular viability. Moreover, increased reactive oxygen species (ROS)-mediated oxidative stress in the TNF-α-treated group enhanced excessive mitochondrial fragmentation and disrupted mitochondrial function. However, treatment with antioxidant N-acetyl cysteine (NAC) or mitochondrial division inhibitor Mdivi-1 protected the cells from these adverse phenomena. These findings provide new insights into the role of the Drp1-dependent mitochondrial pathway in the osteogenic dysfunction during inflammation, indicating that this pathway may be a target for the development of new therapeutic approaches for the prevention and treatment of inflammation-induced bone destruction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Drp1-dependent mitochondrial fission mediates osteogenic dysfunction in inflammation through elevated production of reactive oxygen species

Zhang¹,

Gan²,

He³

et al. 2017

PLoS ONE

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“…Mitochondrial respiration is an important indicator of cell activity and viability that is closely associated with organismal metabolic health and disease [1,2]. Cellular oxygen consumption is linked to energy metabolism by oxidative phosphorylation, the coupling of metabolic substrate oxidation to the production of adenosine triphosphate (ATP) in mitochondria.…”

Section: Introductionmentioning

confidence: 99%

Monitoring oocyte/embryo respiration using electrochemical-based oxygen sensors

Obeidat

Evans

Tedjo

et al. 2018

Sensors and Actuators B: Chemical

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Current commercially available instruments for monitoring mitochondrial respiration are incapable of single cell measurements. Therefore, we developed a three-electrode, Clark-type biosensor suitable for mitochondrial respirometry in single oocytes and embryos. The biosensor was embedded in a PMMA (polymethyl methacrylate) micro-chamber to allow investigation of single oocytes/embryos immersed in up to 100 µL of respiration buffer. The micro-chamber was completely sealed to avoid oxygen exchange between the inside of the chamber and the atmosphere, while being maintained at a temperature of 38.5 ˚C to preserve cell viability. Using amperometry, the oxygen consumption of cells inside the micro-chamber was measured as a change in output current and converted to femto-mol (fmol) oxygen consumed per second based on calibrations with known buffer oxygen concentrations. The sensor measured basal cell respiration supported by endogenous substrates, respiration associated with proton leak induced by inhibition of the adenosine triphosphate (ATP) synthase (complex V) with oligomycin, and the maximal noncoupled respiratory capacity revealed by Carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP) titration. Some potential applications of this oxygen sensor system include evaluating effects of metabolic therapies on oocyte bioenergetics, and monitoring mitochondrial function throughout oocyte maturation and blastocyst development to predict embryo viability to compliment assisted reproductive technologies.

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“…Disturbances in the mitochondria can also cause neurodegenerative diseases, such as Alzheimer's, Parkinson's, Huntington's, and Amyotrophic lateral sclerosis (ALS) (Bernardini et al, 2016;Murphy & Hartley, 2018;Ren et al, 2020). It has been shown that changes in mtDNA registered in the cells of the brain, heart and skeletal muscles in humans (Tokarz & Blasiak, 2014) may be the cause of muscle weakness, neurological diseases or lactic acidosis (Chang et al, 2015;Durhuus et al, 2014). It has been reported that as many as 72-85% of various pathological conditions may be the cause of mitochondrial abnormalities, including mutations in the nDNA, as most mitochondrial proteins are encoded by nDNA (Pronicka et al, 2008;Tońska et al, 2018).…”

mentioning

confidence: 99%

“…Moreover, there are assumptions that disturbances in the delivery of ATP which is produced in the mitochondria to the brain cells may contribute to an increased susceptibility to migraine attacks (Fila et al, 2018). One of the common pathologies closely related to mitochondrial dysfunction in humans is the Lefora's disease which manifests itself in progressive myoclinic epilepsy, ataxia, psychosis and dementia, which may also occur as a result of pathological activation of the p53 protein (Durhuus et al, 2014). Impairment of mitochondrial function in humans is also associated with formation of insulin resistance, as reduced biogenesis of mitochondrial proteins and inhibition of oxidative protein activity leads to accumulation of fatty acids, including diacylglycerols and ceramides that can inhibit insulin signaling (Montgomery & Turner, 2015;Murphy & Hartley, 2018).…”

mentioning

confidence: 99%

Mitochondria, pattern recognition receptors and autophagy under physiological and pathological conditions, including viral infections

et al. 2021

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Research on the health of mammals invariably shows how dynamic immunology is and how the role of many elements and immune processes of the macroorganism, developed in the process of evolution in protecting against threats, including infections, is changing. Among these elements conditioning the homeostasis of the macroorganism are mitochondria, PRR receptors (pattern recognition receptors) and the phenomenon of autophagy. In the context of physiological and pathological states in the body, mitochondria perform various functions. The primary function of these organelles is to produce energy in the cell, but on the other hand, they are heavily involved in various cellular processes, including ROS production and calcium homeostasis. They are largely involved in the activation of immune mechanisms during infectious and non-infectious conditions through mtDNA and the mitochondrial MAVS protein. Mitochondrial involvement has been also determined in PRR-related mechanisms as mtDNA has the ability to directly stimulate TLRs. On the other hand, mitochondria are also associated with apoptotic cell death and autophagy.

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Mitochondria in Health and Disease – 3rd Annual Conference of Society for Mitochondrial Research and Medicine – 19–20 December 2013 — Bengaluru, India

Cited by 5 publications

References 29 publications

Drp1-dependent mitochondrial fission mediates osteogenic dysfunction in inflammation through elevated production of reactive oxygen species

Drp1-dependent mitochondrial fission mediates osteogenic dysfunction in inflammation through elevated production of reactive oxygen species

Monitoring oocyte/embryo respiration using electrochemical-based oxygen sensors

Mitochondria, pattern recognition receptors and autophagy under physiological and pathological conditions, including viral infections

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