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Mitochondrial pharmacology

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https://www.readbyqxmd.com/read/29341928/a-novel-brown-adipocyte-enriched-long-non-coding-rna-that-is-required-for-brown-adipocyte-differentiation-and-sufficient-to-drive-thermogenic-gene-program-in-white-adipocytes
#1
Yan Xiong, Feng Yue, Zhihao Jia, Yun Gao, Wen Jin, Keping Hu, Yong Zhang, Dahai Zhu, Gongshe Yang, Shihuan Kuang
The thermogenic activities of brown and beige adipocytes can be exploited to reduce energy surplus and counteract obesity. Recent RNA sequencing studies have uncovered a number of long noncoding RNAs (lncRNAs) uniquely expressed in white and brown adipose tissues (WAT and BAT), but whether and how these lncRNAs function in adipogenesis remain largely unknown. Here, we report the identification of a novel brown adipocyte-enriched LncRNA (AK079912), and its nuclear localization, function and regulation. The expression of AK079912 increases during brown preadipocyte differentiation and in response to cold-stimulated browning of white adipocytes...
January 13, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29341150/effect-of-akt-activation-and-experimental-pharmacological-inhibition-on-responses-to-neoadjuvant-chemoradiotherapy-in-rectal-cancer
#2
F C Koyama, C M Lopes Ramos, F Ledesma, V A F Alves, J M Fernandes, B B Vailati, G P São Julião, A Habr-Gama, J Gama-Rodrigues, R O Perez, A A Camargo
BACKGROUND: Neoadjuvant chemoradiotherapy (CRT) is one of the preferred initial treatment strategies for locally advanced rectal cancer. Responses are variable, and most patients still require surgery. The aim of this study was to identify molecular mechanisms determining poor response to CRT. METHODS: Global gene expression and pathway enrichment were assessed in pretreatment biopsies from patients with non-metastatic cT2-4 N0-2 rectal cancer within 7 cm of the anal verge...
January 2018: British Journal of Surgery
https://www.readbyqxmd.com/read/29340871/neurotoxicity-of-prosopis-juliflora-from-natural-poisoning-to-mechanism-of-action-of-its-piperidine-alkaloids
#3
Victor Diogenes Amaral da Silva, André Mario Mendes da Silva, Juliana Helena Castro E Silva, Silvia Lima Costa
Prosopis juliflora was introduced in northeastern Brazil in the 1940s, and since then, it has been available as an alternative for animal nutrition. However, the consumption of P. juliflora as main or sole source of food causes an illness in animals known locally as "cara torta" disease. Cattle and goats experimentally intoxicated presents neurotoxic damage in the central nervous system. Histologic lesions were mainly characterized by vacuolation and loss of neurons in trigeminal motor nuclei. Furthermore, mitochondrial damage in neurons and gliosis was reported in trigeminal nuclei of intoxicated cattle...
January 16, 2018: Neurotoxicity Research
https://www.readbyqxmd.com/read/29340048/alteration-of-mitochondrial-biogenesis-promotes-disease-progression-in-multiple-myeloma
#4
Xin Zhan, Wenjie Yu, Reinaldo Franqui-Machin, Melissa L Bates, Kalyan Nadiminti, Huojun Cao, Brad A Amendt, Yogesh Jethava, Ivana Frech, Fenghuang Zhan, Guido Tricot
Many cancers, including multiple myeloma (MM), retain more cytosolic iron to promote tumor cell growth and drug resistance. Higher cytosolic iron promotes oxidative damage due to its interaction with reactive oxygen species generated by mitochondria. The variation of mitochondrial biogenesis in different stages of MM disease was evaluated using gene expression profiles in a large clinical dataset. Sixteen of 18mitochondrial biogenesis related gene sets, including mitochondrial biogenesis signature and oxidative phosphorylation, were increased in myeloma cells compared with normal plasma cells and high expression was associated with an inferior patient outcome...
December 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29338042/a-pharmacological-screen-for-compounds-that-rescue-the-developmental-lethality-of-a-drosophila-atm-mutant
#5
Stacey A Rimkus, David A Wassarman
Ataxia-telangiectasia (A-T) is a neurodegenerative disease caused by mutation of the A-T mutated (ATM) gene. ATM encodes a protein kinase that is activated by DNA damage and phosphorylates many proteins, including those involved in DNA repair, cell cycle control, and apoptosis. Characteristic biological and molecular functions of ATM observed in mammals are conserved in Drosophila melanogaster. As an example, conditional loss-of-function ATM alleles in flies cause progressive neurodegeneration through activation of the innate immune response...
2018: PloS One
https://www.readbyqxmd.com/read/29337205/increasing-mtdna-levels-as-therapy-for-mitochondrial-optic-neuropathies
#6
Eduardo Ruiz-Pesini, Sonia Emperador, Ester López-Gallardo, Carmen Hernandez-Ainsa, Julio Montoya
Leber hereditary optic neuropathy (LHON) is a rare, inherited mitochondrial disease. No treatment has shown a clear-cut benefit on a clinically meaningful end-point. Primary open-angle glaucoma is a frequent, acquired optic neuropathy. Lowering intraocular pressure reduces disease progression. However, current methods to decelerate this progression are recognized as being inadequate. Therefore, there is a clear need to look for new therapeutic approaches. The growing evidence indicates that primary open-angle glaucoma can also be a mitochondrial optic neuropathy (MON)...
January 11, 2018: Drug Discovery Today
https://www.readbyqxmd.com/read/29335845/carnosic-acid-as-a-promising-agent-in-protecting-mitochondria-of-brain-cells
#7
REVIEW
Marcos Roberto de Oliveira
Carnosic acid (CA; C20H28O4), a phenolic diterpene characterized as an ortho-dihydroquinone-type molecule, is a pro-electrophile agent that becomes an electrophile after reacting with free radicals. The electrophile generated from CA interacts with and activates the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor, which is a major modulator of redox biology in mammalian cells. CA induces antioxidant and anti-inflammatory effects in several cell types, as observed in both in vitro and in vivo experimental models...
January 15, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29335542/compartmentalized-activities-of-the-pyruvate-dehydrogenase-complex-sustain-lipogenesis-in-prostate-cancer
#8
Jingjing Chen, Ilaria Guccini, Diletta Di Mitri, Daniela Brina, Ajinkya Revandkar, Manuela Sarti, Emiliano Pasquini, Abdullah Alajati, Sandra Pinton, Marco Losa, Gianluca Civenni, Carlo V Catapano, Jacopo Sgrignani, Andrea Cavalli, Rocco D'Antuono, John M Asara, Andrea Morandi, Paola Chiarugi, Sara Crotti, Marco Agostini, Monica Montopoli, Ionica Masgras, Andrea Rasola, Ramon Garcia-Escudero, Nicolas Delaleu, Andrea Rinaldi, Francesco Bertoni, Johann de Bono, Arkaitz Carracedo, Andrea Alimonti
The mechanisms by which mitochondrial metabolism supports cancer anabolism remain unclear. Here, we found that genetic and pharmacological inactivation of pyruvate dehydrogenase A1 (PDHA1), a subunit of the pyruvate dehydrogenase complex (PDC), inhibits prostate cancer development in mouse and human xenograft tumor models by affecting lipid biosynthesis. Mechanistically, we show that in prostate cancer, PDC localizes in both the mitochondria and the nucleus. Whereas nuclear PDC controls the expression of sterol regulatory element-binding transcription factor (SREBF)-target genes by mediating histone acetylation, mitochondrial PDC provides cytosolic citrate for lipid synthesis in a coordinated manner, thereby sustaining anabolism...
January 15, 2018: Nature Genetics
https://www.readbyqxmd.com/read/29332355/antitumor-activity-of-4-o-methylhonokiol-in-human-oral-cancer-cells-is-mediated-via-ros-generation-disruption-of-mitochondrial-potential-cell-cycle-arrest-and-modulation-of-bcl-2-bax-proteins
#9
Sha Xiao, Fan Chen, Chengzhi Gao
PURPOSE: The plant-derived natural product 4-O-methylhonokiol (MH) has been reported to possess tremendous pharmacological potential ranging from neuroprotection to anticancer activity. However, the anticancer activity of MH in oral squamous cell carcinoma (OSCC) cells has not been evaluated. In the present study, MH was evaluated for its anticancer activity against OSSC PE/CA-PJ41 cells and the possible underlying mechanism was determined. METHODS: Cell cytotoxicity was evaluated by colorimetrybased MTT assay while the effects on cell cycle phase distribution were assessed by flow cytometry...
November 2017: Journal of B.U.ON.: Official Journal of the Balkan Union of Oncology
https://www.readbyqxmd.com/read/29331761/prevention-of-articular-cartilage-degeneration-in-a-rat-model-of-monosodium-iodoacetate-induced-osteoarthritis-by-oral-treatment-with-withaferin-a
#10
Dharmendra Choudhary, Sulekha Adhikary, Naseer Ahmad, Priyanka Kothari, Ashwni Verma, Prabodh Kumar Trivedi, Prabhat Ranjan Mishra, Ritu Trivedi
Withaferin A (WFA), a highly oxygenated withanolide is used for anti-osteoporotic, fracture healing, obesity control as medicine and dietary supplement in Ayurveda and Unani medicine but its potential remains to be investigate for the osteoarthritis studies. In the present study, chondro-protective effects of WFA, under in vitro and in vivo conditions were evaluated. In-vitro pharmacological activity of WFA was tested on rat articular chondrocytes through MTT, DPPH, different staining, FACS and translation studies...
January 10, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29330687/evaluation-of-the-mitochondria-related-redox-and-bioenergetics-effects-of-gastrodin-in-sh-sy5y-cells-exposed-to-hydrogen-peroxide
#11
Marcos Roberto de Oliveira, Flávia Bittencourt Brasil, Cristina Ribas Fürstenau
Mitochondrion is the main site of ATP production in animal cells and also orchestrates signaling pathways associated with cell survival and death. Mitochondrial dysfunction has been linked to bioenergetics and redox impairment in human diseases, such as neurodegeneration and cardiovascular disease. Protective agents able to attenuate mitochondrial impairment are of pharmacological interest. Gastrodin (GAS; 4-hydroxybenzyl alcohol 4-O-beta-D-glucoside) is a phenolic glucoside obtained from the Chinese herbal medicine Gastrodia elata Blume and exhibits antioxidant, anti-inflammatory, and antiapoptotic effects in several cell types...
January 12, 2018: Journal of Molecular Neuroscience: MN
https://www.readbyqxmd.com/read/29329795/omega-3-fatty-acids-and-adipose-tissue-biology
#12
REVIEW
Ondrej Kuda, Martin Rossmeisl, Jan Kopecky
This review provides evidence for the importance of white and brown adipose tissue (i.e. WAT and BAT) function for the maintenance of healthy metabolic phenotype and its preservation in response to omega-3 polyunsaturated fatty acids (omega-3 PUFA), namely in the context of diseased states linked to aberrant accumulation of body fat, systemic low-grade inflammation, dyslipidemia and insulin resistance. More specifically, the review deals with (i) the concept of immunometabolism, i.e. how adipose-resident immune cells and adipocytes affect each other and define the immune-metabolic interface; and (ii) the characteristic features of "healthy adipocytes" in WAT, which are relatively small fat cells endowed with a high capacity for mitochondrial oxidative phosphorylation, triacylglycerol/fatty acid (TAG/FA) cycling and de novo lipogenesis (DNL)...
January 9, 2018: Molecular Aspects of Medicine
https://www.readbyqxmd.com/read/29326403/resveratrol-an-nrf2-activator-ameliorates-aging-related-progressive-renal-injury
#13
Eun Nim Kim, Ji Hee Lim, Min Young Kim, Tae Hyun Ban, In-Ae Jang, Hye Eun Yoon, Cheol Whee Park, Yoon Sik Chang, Bum Soon Choi
BACKGROUND: Two important issues in the aging kidney are mitochondrial dysfunction and oxidative stress. An Nrf2 activator, resveratrol, is known to have various effects. Resveratrol may prevent inflammation and oxidative stress by activating Nrf2 and SIRT1 signaling. We examined whether resveratrol could potentially ameliorate the cellular condition, such as renal injury due to cellular oxidative stress and mitochondrial dysfunction caused by aging. METHODS: Male 18-month-old C57BL/6 mice were used...
January 11, 2018: Aging
https://www.readbyqxmd.com/read/29325869/microglial-activation-and-the-nitric-oxide-cgmp-pkg-pathway-underlie-enhanced-neuronal-vulnerability-to-mitochondrial-dysfunction-in-experimental-multiple-sclerosis
#14
Andrea Mancini, Michela Tantucci, Petra Mazzocchetti, Antonio de Iure, Valentina Durante, Lara Macchioni, Carmela Giampà, Alessandra Alvino, Lorenzo Gaetani, Cinzia Costa, Alessandro Tozzi, Paolo Calabresi, Massimiliano Di Filippo
During multiple sclerosis (MS), a close link has been demonstrated to occur between inflammation and neuro-axonal degeneration, leading to the hypothesis that immune mechanisms may promote neurodegeneration, leading to irreversible disease progression. Energy deficits and inflammation-driven mitochondrial dysfunction seem to be involved in this process. In this work we investigated, by the use of striatal electrophysiological field-potential recordings, if the inflammatory process associated with experimental autoimmune encephalomyelitis (EAE) is able to influence neuronal vulnerability to the blockade of mitochondrial complex IV, a crucial component for mitochondrial activity responsible of about 90% of total cellular oxygen consumption...
January 8, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29325568/pink1-import-regulation-a-fine-system-to-convey-mitochondrial-stress-to-the-cytosol
#15
REVIEW
Shiori Sekine, Richard J Youle
Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway...
January 10, 2018: BMC Biology
https://www.readbyqxmd.com/read/29323772/the-role-of-nrf2-signaling-in-counteracting-neurodegenerative-diseases
#16
REVIEW
Albena T Dinkova-Kostova, Rumen V Kostov, Aleksey G Kazantsev
The transcription factor Nrf2 (nuclear factor erythroid 2 p45-related factor 2) functions at the interface of cellular redox and intermediary metabolism. Nrf2 target genes encode antioxidant enzymes, and proteins involved in xenobiotic detoxification, repair and removal of damaged proteins and organelles, inflammation, and mitochondrial bioenergetics. The function of Nrf2 is altered in many neurodegenerative disorders, such as Huntington's disease, Alzheimer's disease, amyotrophic lateral sclerosis and Friedreich's ataxia...
January 11, 2018: FEBS Journal
https://www.readbyqxmd.com/read/29323117/impaired-autophagy-bridges-lysosomal-storage-disease-and-epithelial-dysfunction-in-the-kidney
#17
Beatrice Paola Festa, Zhiyong Chen, Marine Berquez, Huguette Debaix, Natsuko Tokonami, Jenny Ann Prange, Glenn van de Hoek, Cremonesi Alessio, Andrea Raimondi, Nathalie Nevo, Rachel H Giles, Olivier Devuyst, Alessandro Luciani
The endolysosomal system sustains the reabsorptive activity of specialized epithelial cells. Lysosomal storage diseases such as nephropathic cystinosis cause a major dysfunction of epithelial cells lining the kidney tubule, resulting in massive losses of vital solutes in the urine. The mechanisms linking lysosomal defects and epithelial dysfunction remain unknown, preventing the development of disease-modifying therapies. Here we demonstrate, by combining genetic and pharmacologic approaches, that lysosomal dysfunction in cystinosis results in defective autophagy-mediated clearance of damaged mitochondria...
January 11, 2018: Nature Communications
https://www.readbyqxmd.com/read/29319901/gomisin-a-modulates-aging-progress-via-mitochondrial-biogenesis-in-human-diploid-fibroblast-cells
#18
Jeong-Seok Kim, Seon-Hwa Jeong, Sin-Hee Han, Ho-Keun Yi
Gomisin A from the fruit of Schisandra chinensis has many pharmacological properties, including hepato-protective, anti-diabetic, and anti-oxidative stress. However, the potential benefit of gomisin A is still not well understood, especially in aging progression. Therefore, the aim of this study was to clarify whether the promotion of mitochondrial biogenesis and autophagy of gomisin A affects anti-aging progression, and its mechanism. Intermediate (PD32) Human diploid fibroblast (HDF) cells were brought to stress-induced premature senescence (SIPS) using hydrogen peroxide (H2 O2 )...
January 10, 2018: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/29319185/pharmacological-modulation-of-mitochondrial-calcium-homeostasis
#19
Daniela M Arduino, Fabiana Perocchi
Mitochondria are pivotal organelles in calcium (Ca2+ ) handling and signalling, constituting intracellular checkpoints for numerous processes that are vital for cell life. Alterations in mitochondrial Ca2+ homeostasis have been linked to a variety of pathological conditions and are critical in the etiology of several human diseases. Efforts have been taken to harness mitochondrial Ca2+ transport mechanisms for therapeutic intervention but pharmacological compounds that direct and selectively modulate mitochondrial Ca2+ homeostasis are currently lacking...
January 10, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29317678/peptidomimetic-blockade-of-myb-in-acute-myeloid-leukemia
#20
Kavitha Ramaswamy, Lauren Forbes, Gerard Minuesa, Tatyana Gindin, Fiona Brown, Michael G Kharas, Andrei V Krivtsov, Scott A Armstrong, Eric Still, Elisa de Stanchina, Birgit Knoechel, Richard Koche, Alex Kentsis
Aberrant gene expression is a hallmark of acute leukemias. MYB-driven transcriptional coactivation with CREB-binding protein (CBP)/P300 is required for acute lymphoblastic and myeloid leukemias, including refractory MLL-rearranged leukemias. Using structure-guided molecular design, we developed a peptidomimetic inhibitor MYBMIM that interferes with the assembly of the molecular MYB:CBP/P300 complex and rapidly accumulates in the nuclei of AML cells. Treatment of AML cells with MYBMIM led to the dissociation of the MYB:CBP/P300 complex in cells, its displacement from oncogenic enhancers enriched for MYB binding sites, and downregulation of MYB-dependent gene expression, including of MYC and BCL2 oncogenes...
January 9, 2018: Nature Communications
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