keyword
MENU ▼
Read by QxMD icon Read
search

Mitochondrial health

keyword
https://www.readbyqxmd.com/read/28928628/axonal-degeneration-during-aging-and-its-functional-role-in-neurodegenerative-disorders
#1
REVIEW
Natalia Salvadores, Mario Sanhueza, Patricio Manque, Felipe A Court
Aging constitutes the main risk factor for the development of neurodegenerative diseases. This represents a major health issue worldwide that is only expected to escalate due to the ever-increasing life expectancy of the population. Interestingly, axonal degeneration, which occurs at early stages of neurodegenerative disorders (ND) such as Alzheimer's disease, Amyotrophic lateral sclerosis, and Parkinson's disease, also takes place as a consequence of normal aging. Moreover, the alteration of several cellular processes such as proteostasis, response to cellular stress and mitochondrial homeostasis, which have been described to occur in the aging brain, can also contribute to axonal pathology...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28926527/genistein-suppresses-aerobic-glycolysis-and-induces-hepatocellular-carcinoma-cell-death
#2
Sainan Li, Jingjing Li, Weiqi Dai, Qinghui Zhang, Jiao Feng, Liwei Wu, Tong Liu, Qiang Yu, Shizan Xu, Wenwen Wang, Xiya Lu, Kan Chen, Yujing Xia, Jie Lu, Yingqun Zhou, Xiaoming Fan, Wenhui Mo, Ling Xu, Chuanyong Guo
BACKGROUND: Genistein is a natural isoflavone with many health benefits, including antitumour effects. Increased hypoxia-inducible factor 1 α (HIF-1α) levels and glycolysis in tumour cells are associated with an increased risk of mortality, cancer progression, and resistance to therapy. However, the effect of genistein on HIF-1α and glycolysis in hepatocellular carcinoma (HCC) is still unclear. METHODS: Cell viability, apoptosis rate, lactate production, and glucose uptake were measured in HCC cell lines with genistein incubation...
September 19, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/28924745/hypertonia-linked-protein-trak1-functions-with-mitofusins-to-promote-mitochondrial-tethering-and-fusion
#3
Crystal A Lee, Lih-Shen Chin, Lian Li
Hypertonia is a neurological dysfunction associated with a number of central nervous system disorders, including cerebral palsy, Parkinson's disease, dystonia, and epilepsy. Genetic studies have identified a homozygous truncation mutation in Trak1 that causes hypertonia in mice. Moreover, elevated Trak1 protein expression is associated with several types of cancers and variants in Trak1 are linked to childhood absence epilepsy in humans. Despite the importance of Trak1 in health and disease, the mechanisms of Trak1 action remain unclear and the pathogenic effects of Trak1 mutation are unknown...
September 18, 2017: Protein & Cell
https://www.readbyqxmd.com/read/28918113/regulation-of-mitochondrial-bioenergetics-by-the-non-canonical-roles-of-mitochondrial-dynamics-proteins-in-the-heart
#4
REVIEW
Wang Wang, Celia Fernandez-Sanz, Shey-Shing Sheu
Recent advancement in mitochondrial research has significantly extended our knowledge on the role and regulation of mitochondria in health and disease. One important breakthrough is the delineation of how mitochondrial morphological changes, termed mitochondrial dynamics, are coupled to the bioenergetics and signaling functions of mitochondria. In general, it is believed that fusion leads to an increased mitochondrial respiration efficiency and resistance to stress-induced dysfunction while fission does the contrary...
September 13, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28917714/mitochondria-in-the-nervous-system-from-health-to-disease-part-i
#5
EDITORIAL
Brian M Polster, Maria Teresa Carrì, Philip M Beart
In Part I of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together contributions from experts in brain mitochondrial research to provide an up-to-date overview of mitochondrial functioning in physiology and pathology. The issue provides cutting edge reviews on classical areas of mitochondrial biology that include energy substrate utilization, calcium handling, mitochondria-endoplasmic reticulum communication, and cell death regulation. Additional reviews and original research articles touch upon key mitochondrial defects seen across multiple neurodegenerative conditions, including fragmentation, loss of respiratory capacity, calcium overload, elevated reactive oxygen species generation, perturbed NAD(+) metabolism, altered protein acetylation, and compromised mitophagy...
September 13, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28916822/ampk-phosphorylation-of-ulk1-is-required-for-targeting-of-mitochondria-to-lysosomes-in-exercise-induced-mitophagy
#6
Rhianna C Laker, Joshua C Drake, Rebecca J Wilson, Vitor A Lira, Bevan M Lewellen, Karen A Ryall, Carleigh C Fisher, Mei Zhang, Jeffrey J Saucerman, Laurie J Goodyear, Mondira Kundu, Zhen Yan
Mitochondrial health is critical for skeletal muscle function and is improved by exercise training through both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy. The mechanisms underlying exercise-induced mitophagy have not been fully elucidated. Here, we show that acute treadmill running in mice causes mitochondrial oxidative stress at 3-12 h and mitophagy at 6 h post-exercise in skeletal muscle. These changes were monitored using a novel fluorescent reporter gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosphorylation of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kinase 1 (Ulk1) at serine 555...
September 15, 2017: Nature Communications
https://www.readbyqxmd.com/read/28915507/ambient-fine-particulate-matters-induce-cell-death-and-inflammatory-response-by-influencing-mitochondria-function-in-human-corneal-epithelial-cells
#7
Eun-Jung Park, Jae-Byoung Chae, Jungmook Lyu, Cheolho Yoon, Sanghwa Kim, Changjoo Yeom, Younghun Kim, Jaerak Chang
Ambient fine particulate matter (AFP) is a main risk factor for the cornea as ultraviolet light. However, the mechanism of corneal damage following exposure to AFP has been poorly understood. In this study, we first confirmed that AFP can penetrate the cornea of mice, considering that two-dimensional cell culture systems are limited in reflecting the situation in vivo. Then, we investigated the toxic mechanism using human corneal epithelial (HCET) cells. At 24h after exposure, AFP located within the autophagosome-like vacuoles, and cell proliferation was clearly inhibited in all the tested concentration...
September 12, 2017: Environmental Research
https://www.readbyqxmd.com/read/28915355/thiamin-deficiency-on-fetal-brain-development-with-and-without-prenatal-alcohol-exposure
#8
Olena Kloss, Michael Eskin, Miyoung Suh
Adequate thiamin levels are crucial for optimal health, through maintenance of homeostasis and viability of metabolic enzymes, which require thiamine as a co-factor. Thiamin deficiency occurs during pregnancy when dietary intake is inadequate or excessive alcohol is consumed. Thiamin deficiency leads to brain dysfunction due to its involvement in synthesis of myelin and neurotransmitters (eg. acetylcholine, γ-aminobutyric acid, glutamate), and increases oxidative stress by decreasing the production of reducing agents...
September 15, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/28915327/adipose-tissue-in-hiv-infection
#9
John R Koethe
HIV infection and antiretroviral therapy (ART) treatment exert diverse effects on adipocytes and stromal-vascular fraction cells, leading to changes in adipose tissue quantity, distribution, and energy storage. A HIV-associated lipodystrophic condition was recognized early in the epidemic, characterized by clinically apparent changes in subcutaneous, visceral, and dorsocervical adipose depots. Underlying these changes is altered adipose tissue morphology and expression of genes central to adipocyte maturation, regulation, metabolism, and cytokine signaling...
September 12, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28906435/mitochondrial-biogenesis-in-response-to-chromium-vi-toxicity-in-human-liver-cells
#10
Xiali Zhong, Rita de Cássia da Silveira E Sá, Caigao Zhong
Hexavalent chromium (Cr(VI)) is a ubiquitous environmental pollutant, which poses a threat to human public health. Recent studies have shown that mitochondrial biogenesis can be activated by inflammatory and oxidative stress. However, whether mitochondrial biogenesis is involved in Cr(VI)-induced hepatotoxicity is unclear. Here, we demonstrated the induction of inflammatory response and oxidative stress, as indicated by upregulation of inflammatory factors and reactive oxygen species (ROS). Subsequently, we demonstrated that mitochondrial biogenesis, comprising the mitochondrial DNA copy number and mitochondrial mass, was significantly increased in HepG2 cells exposed to low concentrations of Cr(VI)...
September 14, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28901341/-healthcare-services-citizen-s-right-and-healthcare-systems-safeguard-considerations-rising-from-the-charlie-gard-story
#11
Giuseppe R Gristina
The story of Charlie Gard, an 11-month-old boy suffering from a rare inherited mitochondrial disease called 'infantile encephalomyopathic mitochondrial DNA depletion syndrome' and kept alive thanks to life supports, rises some issues regarding the provision of healthcare. Is there a right of an individual person to buy any healthcare benefits only because he has enough money to do so? If the answer is 'yes', in light of the distributive justice principle how do governments balance this right with the obligation to regulate health care systems ensuring that all treatments are useful and affordable for everybody? Many considerations of the best interest of patients can be found in this debate, but we cannot ignore neither the value of the scientific method as the cornerstone of the medical profession nor a commitment to support the moral integrity of clinical practice by refusing to provide treatments that do not meet a reasonable threshold of scientific justification evidence-based...
September 2017: Recenti Progressi in Medicina
https://www.readbyqxmd.com/read/28899781/direct-effects-of-mitochondrial-dysfunction-on-poor-bone-health-in-leigh-syndrome
#12
Hiroki Kato, Xu Han, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Hiroshi Sato, Thanh Thi Mai Pham, Tomoaki Taguchi, Kazuaki Nonaka
Mitochondrial diseases are the result of aberrant mitochondrial function caused by mutations in either nuclear or mitochondrial DNA. Poor bone health has recently been suggested as a symptom of mitochondrial diseases; however, a direct link between decreased mitochondrial function and poor bone health in mitochondrial disease has not been demonstrated. In this study, stem cells from human exfoliated deciduous teeth (SHED) were isolated from a child with Leigh syndrome (LS), a mitochondrial disease, and the effects of decreased mitochondrial function on poor bone health were analyzed...
September 9, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28892826/increased-mortality-and-comorbidity-associated-with-leber-s-hereditary-optic-neuropathy-a-nationwide-cohort-study
#13
Nanna Vestergaard, Thomas Rosenberg, Christian Torp-Pedersen, Henrik Vorum, Carl U Andersen, Kristian Aasbjerg
Purpose: Leber's hereditary optic neuropathy (LHON) is a mitochondrial genetic disease in which optic neuropathy is considered a key feature. Several other manifestations of LHON have been reported; however, only little is known of their incidence and the life expectancy in LHON patients. Methods: This study, based on Danish nationwide health registries, included 141 patients diagnosed with LHON and 297 unaffected family members in the maternal line. The incidence of comorbidities and mortality for patients with LHON and unaffected family members was compared with that in the general population...
September 1, 2017: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/28892507/extreme-genome-diversity-in-the-hyper-prevalent-parasitic-eukaryote-blastocystis
#14
Eleni Gentekaki, Bruce A Curtis, Courtney W Stairs, Vladimír Klimeš, Marek Eliáš, Dayana E Salas-Leiva, Emily K Herman, Laura Eme, Maria C Arias, Bernard Henrissat, Frédérique Hilliou, Mary J Klute, Hiroshi Suga, Shehre-Banoo Malik, Arthur W Pightling, Martin Kolisko, Richard A Rachubinski, Alexander Schlacht, Darren M Soanes, Anastasios D Tsaousis, John M Archibald, Steven G Ball, Joel B Dacks, C Graham Clark, Mark van der Giezen, Andrew J Roger
Blastocystis is the most prevalent eukaryotic microbe colonizing the human gut, infecting approximately 1 billion individuals worldwide. Although Blastocystis has been linked to intestinal disorders, its pathogenicity remains controversial because most carriers are asymptomatic. Here, the genome sequence of Blastocystis subtype (ST) 1 is presented and compared to previously published sequences for ST4 and ST7. Despite a conserved core of genes, there is unexpected diversity between these STs in terms of their genome sizes, guanine-cytosine (GC) content, intron numbers, and gene content...
September 11, 2017: PLoS Biology
https://www.readbyqxmd.com/read/28891792/pgam5-promotes-lasting-foxo-activation-after-developmental-mitochondrial-stress-and-extends-lifespan-in-drosophila
#15
Martin Borch Jensen, Yanyan Qi, Rebeccah Riley, Liya Rabkina, Heinrich Jasper
The mitochondrial unfolded protein response (UPR(mt)) has been associated with long lifespan across metazoans. In C. elegans, mild developmental mitochondrial stress activates UPR(mt) reporters and extends lifespan. We show that similar developmental stress is necessary and sufficient to extend Drosophila lifespan, and identify Phosphoglycerate Mutase 5 (PGAM5) as a mediator of this response. Developmental mitochondrial stress leads to activation of FoxO, via Apoptosis Signal-regulating Kinase 1 (ASK1) and Jun-N-terminal Kinase (JNK)...
September 11, 2017: ELife
https://www.readbyqxmd.com/read/28890349/molecular-hydrogen-modulates-gene-expression-via-histone-modification-and-induces-the-mitochondrial-unfolded-protein-response
#16
Sayaka Sobue, Chisato Inoue, Fumiko Hori, Shanlou Qiao, Takashi Murate, Masatoshi Ichihara
Molecular hydrogen (H2) is a biologically active gas that is used medically to ameliorate various systemic pathological conditions. H2 also regulates gene expression involved in intracellular signaling and metabolic pathways. However, it is unclear whether H2 affects gene expression directly or through indirect effects as a consequence of health improvement. Therefore, we attempted to identify genes that exhibit similar changes in expression in response to H2 by employing DNA microarrays and gene set enrichment analysis to analyze RNA from liver and lung of rats and mice with or without dietary stress...
September 7, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28890317/mitoneod-a-mitochondria-targeted-superoxide-probe
#17
Maria M Shchepinova, Andrew G Cairns, Tracy A Prime, Angela Logan, Andrew M James, Andrew R Hall, Sara Vidoni, Sabine Arndt, Stuart T Caldwell, Hiran A Prag, Victoria R Pell, Thomas Krieg, John F Mulvey, Pooja Yadav, James N Cobley, Thomas P Bright, Hans M Senn, Robert F Anderson, Michael P Murphy, Richard C Hartley
Mitochondrial superoxide (O2(⋅-)) underlies much oxidative damage and redox signaling. Fluorescent probes can detect O2(⋅-), but are of limited applicability in vivo, while in cells their usefulness is constrained by side reactions and DNA intercalation. To overcome these limitations, we developed a dual-purpose mitochondrial O2(⋅-) probe, MitoNeoD, which can assess O2(⋅-) changes in vivo by mass spectrometry and in vitro by fluorescence. MitoNeoD comprises a O2(⋅-)-sensitive reduced phenanthridinium moiety modified to prevent DNA intercalation, as well as a carbon-deuterium bond to enhance its selectivity for O2(⋅-) over non-specific oxidation, and a triphenylphosphonium lipophilic cation moiety leading to the rapid accumulation within mitochondria...
August 24, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28887652/disruption-of-adenylyl-cyclase-type-5-mimics-exercise-training
#18
John J Guers, Jie Zhang, Sara C Campbell, Marko Oydanich, Dorothy E Vatner, Stephen F Vatner
Exercise training is key to healthful longevity. Since exercise training compliance is difficult, it would be useful to have a therapeutic substitute that mimicked exercise training. We compared the effects of exercise training in wild-type (WT) littermates with adenylyl cyclase type 5 knock out (AC5 KO) mice, a model of enhanced exercise performance. Exercise performance, measured by maximal distance and work to exhaustion, was increased in exercise-trained WT to levels already attained in untrained AC5 KO...
September 8, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28885978/in-vitro-evaluation-of-mitochondrial-function-and-estrogen-signaling-in-cell-lines-exposed-to-the-antiseptic-cetylpyridinium-chloride
#19
Sandipan Datta, Guochun He, Alexey Tomilov, Sunil Sahdeo, Michael S Denison, Gino Cortopassi
BACKGROUND: Quaternary ammonium salts (QUATS), such as cetylpyridinium chloride (CPC) and benzalkonium chloride (BAK), are frequently used in antiseptic formulations, including toothpastes, mouthwashes, lozenges, throat and nasal sprays, and as biocides. Although in a recent ruling, the U.S. Food and Drug Administration (FDA) banned CPC from certain products and requested more data on BAK's efficacy and safety profile, QUATS, in general, and CPC and BAK, in particular, continue to be used in personal health care, food, and pharmaceutical and cleaning industries...
August 22, 2017: Environmental Health Perspectives
https://www.readbyqxmd.com/read/28882480/short-term-administration-of-nicotinamide-mononucleotide-preserves-cardiac-mitochondrial-homeostasis-and-prevents-heart-failure
#20
Rongli Zhang, Yuyan Shen, Lin Zhou, Panjamaporn Sangwung, Hisashi Fujioka, Lilei Zhang, Xudong Liao
Heart failure is associated with mitochondrial dysfunction so that restoring or improving mitochondrial health is of therapeutic importance. Recently, reduction in NAD(+) levels and NAD(+)-mediated deacetylase activity has been recognized as negative regulators of mitochondrial function. Using a cardiac specific KLF4 deficient mouse line that is sensitive to stress, we found mitochondrial protein hyperacetylation coupled with reduced Sirt3 and NAD(+) levels in the heart before stress, suggesting that the KLF4-deficient heart is predisposed to NAD(+)-associated defects...
September 5, 2017: Journal of Molecular and Cellular Cardiology
keyword
keyword
26112
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"