keyword
MENU ▼
Read by QxMD icon Read
search

Mitochondrial dysfunction

keyword
https://www.readbyqxmd.com/read/29222946/triheptanoin-protects-against-status-epilepticus-induced-hippocampal-mitochondrial-dysfunctions-oxidative-stress-and-neuronal-degeneration
#1
Kah Ni Tan, David Simmons, Catalina Carrasco-Pozo, Karin Borges
Triheptanoin, the triglyceride of heptanoate, is anaplerotic (refills deficient tricarboxylic acid cycle intermediates) via the propionyl-CoA carboxylase (PCC) pathway. It has been shown to be neuroprotective and anticonvulsant in several models of neurological disorders. Here, we investigated the effects of triheptanoin against changes of hippocampal mitochondrial functions, oxidative stress and cell death induced by pilocarpine-induced status epilepticus (SE) in mice. Ten days of triheptanoin pre-treatment did not protect against SE, but it preserved hippocampal mitochondrial functions including state 2, state 3 ADP, state 3 uncoupled respiration, respiration linked to ATP synthesis along with the activities of pyruvate dehydrogenase complex and oxoglutarate dehydrogenase complex 24 h post-SE...
December 9, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29222162/dual-inhibition-of-pik3c3-and-fgfr-as-a-new-therapeutic-approach-to-treat-bladder-cancer
#2
Chun-Han Chen, C Changou, Tsung-Han Hsieh, Yu-Ching Lee, Cheng-Ying Chu, Kai-Cheng Hsu, Hao-Ching Wang, Yu-Chen Lin, Yan-Ni Lo, Yun-Ru Liu, Jing-Ping Liou, Yun Yen
PURPOSE: MPT0L145 has been developed as a FGFR inhibitor exhibiting significant anti-bladder cancer activity in vitro and in vivo via promoting autophagy-dependent cell death. Here, we aim to elucidate the underlying mechanisms. EXPERIMENTAL DESIGN: Autophagy flux, morphology and intracellular organelles were evaluated by western blotting, transmission electron microscope and fluorescence microscope. Molecular docking, surface plasmon resonance assay were performed to identify drug-protein interaction...
December 8, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/29222055/autophagy-plays-a-protective-role-in-mn-induced-toxicity-in-pc12-cells
#3
Qian Zhou, Xiaolong Fu, Xueting Wang, Qin Wu, Yuanfu Lu, Jingshan Shi, James E Klaunig, Shaoyu Zhou
Excessive environmental or occupational exposure to manganese (Mn) is associated with increased risk of neuron degenerative disorders. Oxidative stress and mitochondrial dysfunction are the main mechanisms of Mn mediated neurotoxicity. Selective removal of damaged mitochondria by autophagy has been proposed as a protective mechanism against neuronal toxicant-induced neurotoxicity. Whether autophagic flux plays a role in Mn-induced cytotoxicity remains to be fully elucidated. The present study was designed to investigate the effect of Mn exposure on autophagy, and how modulation of autophagic flux alters the sensitivities of cells to Mn-elicited cytotoxicity...
December 5, 2017: Toxicology
https://www.readbyqxmd.com/read/29221988/modulations-of-keap1-nrf2-signaling-axis-by-tiia-ameliorated-the-oxidative-stress-induced-myocardial-apoptosis
#4
Shi-Hai Yan, Ning-Wei Zhao, Zhi-Rong Geng, Jia-Yin Shen, Fu-Ming Liu, Dong Yan, Jie Zhou, Chao Nie, Cheng-Cai Huang, Zhu-Yuan Fang
Mounting evidence has strongly implicated oxidative stress in the development of cardiac dysfunction, and myocardial apoptosis contributes to the pathogenesis of heart failure. Quantitative cardiac proteomics data revealed that pressure load by TAC resulted in a significant decline in mitochondrial metabolic activity, where TIIA (Tanshinone IIA sulfonate) treatment reversed it in vivo, which might be mediated by Nrf2. In NRVMs, TIIA treatment ameliorated H2O2-induced caspase-3/9 activations through the suppression of p38 and mTOR signaling pathways, where caspase-mediated cleavage of YY1 and PARP resulted in the defects in mitochondrial biogenesis and DNA repair, and this event finally led to cardiomyocyte apoptosis...
December 5, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29221810/mitochondrial-dysfunction-and-damage-associated-molecular-patterns-damps-in-chronic-inflammatory-diseases
#5
REVIEW
Charles S Dela Cruz, Min-Jong Kang
Inflammation represents a comprehensive host response to external stimuli for the purpose of eliminating the offending agent, minimizing injury to host tissues and fostering repair of damaged tissues back to homeostatic levels. In normal physiologic context, inflammatory response culminates with the resolution of infection and tissue damage response. However, in a pathologic context, persistent or inappropriately regulated inflammation occurs that can lead to chronic inflammatory diseases. Recent scientific advances have integrated the role of innate immune response to be an important arm of the inflammatory process...
December 5, 2017: Mitochondrion
https://www.readbyqxmd.com/read/29219755/mitochondrial-abnormalities-related-to-the-dysfunction-of-circulating-endothelial-colony-forming-cells-in-moyamoya-disease
#6
Jung Won Choi, Sung Min Son, Inhee Mook-Jung, Youn Joo Moon, Ji Yeoun Lee, Kyu-Chang Wang, Hyun-Seung Kang, Ji Hoon Phi, Seung Ah Choi, Sangjoon Chong, Jayoung Byun, Seung-Ki Kim
OBJECTIVE Moyamoya disease (MMD) is a unique cerebrovascular disorder characterized by the progressive occlusion of the bilateral internal carotid arteries. Endothelial colony-forming cells (ECFCs), previously termed "endothelial progenitor cells," play an important role in the pathogenesis of MMD. In this study, the authors performed morphological and functional studies of the mitochondria of ECFCs from patients with MMD to present new insights into the pathogenesis of the disease. METHODS The morphology of ECFCs from 5 MMD patients and 5 healthy controls was examined under both a transmission electron microscope and a confocal laser scanning microscope...
December 8, 2017: Journal of Neurosurgery
https://www.readbyqxmd.com/read/29219064/natural-product-formulations-for-prevention-and-treatment-of-alzheimer-s-disease-a-patent-review
#7
Rumiana Koynova, Boris Tenchov
INTRODUCTION: Although considerable efforts have been made to develop effective therapeutic agents for Alzheimer's disease (AD), neither a consensus concerning the pathogenesis of the disease nor a successful therapy for its treatment is available. The natural product chemistry brings tremendous diversity and abundant resource for medical needs. OBJECTIVES: The present review summarizes recent patents on natural extracts and derived drugs as agents for prevention and treatment of AD...
December 7, 2017: Recent Patents on Drug Delivery & Formulation
https://www.readbyqxmd.com/read/29218782/therapy-development-in-huntington-disease-from-current-strategies-to-emerging-opportunities
#8
REVIEW
Audrey S Dickey, Albert R La Spada
Huntington disease (HD) is a progressive autosomal dominant neurodegenerative disorder in which patients typically present with uncontrolled involuntary movements and subsequent cognitive decline. In 1993, a CAG trinucleotide repeat expansion in the coding region of the huntingtin (HTT) gene was identified as the cause of this disorder. This extended CAG repeat results in production of HTT protein with an expanded polyglutamine tract, leading to pathogenic HTT protein conformers that are resistant to protein turnover, culminating in cellular toxicity and neurodegeneration...
December 8, 2017: American Journal of Medical Genetics. Part A
https://www.readbyqxmd.com/read/29218775/comparative-proteomic-analysis-of-silver-nanoparticle-effects-in-human-liver-and-intestinal-cells
#9
Albert Braeuning, Axel Oberemm, Josephine Görte, Linda Böhmert, Sabine Juling, Alfonso Lampen
Consumers are orally exposed to nanoparticulate or soluble species of the non-essential element silver due to its use in food contact materials or as a food additive. Potential toxicity of silver nanoparticles has gained special scientific attention. A fraction of ingested ionic or particulate silver is taken up in the intestine and transported to the liver, where it may induce oxidative stress and elicit subsequent adverse responses. Here, we present a comprehensive analysis of global proteomic changes induced in human Hep G2 hepatocarcinoma cells by different concentrations of AgPURE silver nanoparticles or by corresponding concentrations of ionic silver...
December 7, 2017: Journal of Applied Toxicology: JAT
https://www.readbyqxmd.com/read/29218453/energy-depletion-and-not-ros-formation-is-a-crucial-step-of-glucolipotoxicity-gltx-in-pancreatic-beta-cells
#10
Morgana Barroso Oquendo, Nikolas Layer, Rebecca Wagner, Peter Krippeit-Drews, Gisela Drews
We have shown previously that genetic or pharmacological deletion of KATP channels protect against beta cell dysfunction induced by reactive oxygen species (ROS). Since it is assumed that glucolipotoxicity (GLTx) causes ROS production, we aimed to evaluate whether suppression of KATP channel activity can also prevent beta cell damage evoked by GLTx. We used an in vitro model of GLTx and measured distinct parameters of stimulus-secretion coupling. GLTx gradually induced disturbances of Ca2+ oscillations over 3 days...
December 7, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29218248/propafenone-suppresses-esophageal-cancer-proliferation-through-inducing-mitochondrial-dysfunction
#11
Wei-Bin Zheng, Yang-Jia Li, Yang Wang, Jie Yang, Can-Can Zheng, Xiao-Hui Huang, Bin Li, Qing-Yu He
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors with poor survival and limited therapeutic options. The aim of this study is to identify novel anticancer strategies from existing Food and Drug Administration (FDA)-approved drugs that have been used to clinically treat other diseases. Here, propafenone, an antiarrhythmic medication, was found to induce apoptosis and exert a significantly inhibitory effect on the proliferation and colony-forming ability of ESCC cells in a dose-dependent manner without observed cytotoxicity on normal esophageal epithelial cells...
2017: American Journal of Cancer Research
https://www.readbyqxmd.com/read/29218098/overexpression-of-microrna-145-protects-against-rat-myocardial-infarction-through-targeting-pdcd4
#12
Hao Xu, Heng Cao, Guoqing Zhu, Shaowen Liu, Hongli Li
Myocardial infarction (MI) is a common cardiovascular disease with high mortality. The aim of the present study was to determine the biological role of miR-145 in MI rats and hypoxia-injured cardiomyocytes and to elucidate the potential mechanism. MI rats were induced by left anterior descending artery (LAD) ligation. qRT-PCR and western blot analysis were performed to determine the mRNA and protein levels, respectively. Compared with sham group, miR-145 levels in MI group were significantly decreased. We observed that lentivirus-mediated overexpression of miR-145 significantly improves cardiac function, reduces infarcted tissue size and prevents post-infarction induced apoptosis in rats after MI...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/29217757/novel-mitochondria-targeting-peptide-in-heart-failure-treatment-a-randomized-placebo-controlled-trial-of-elamipretide
#13
Melissa A Daubert, Eric Yow, Gary Dunn, Sotir Marchev, Huiman Barnhart, Pamela S Douglas, Christopher O'Connor, Sidney Goldstein, James E Udelson, Hani N Sabbah
BACKGROUND: Mitochondrial dysfunction and energy depletion in the failing heart are innovative therapeutic targets in heart failure management. Elamipretide is a novel tetrapeptide that increases mitochondrial energy; however, its safety, tolerability, and therapeutic effect on cardiac structure and function have not been studied in heart failure with reduced ejection fraction. METHODS AND RESULTS: In this double-blind, placebo-controlled, ascending-dose trial, patients with heart failure with reduced ejection fraction (ejection fraction, ≤35%) were randomized to either a single 4-hour infusion of elamipretide (cohort 1 [n=8], 0...
December 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/29217634/anthracycline-cardiotoxicity-an-update-on-mechanisms-monitoring-and-prevention
#14
REVIEW
Peter A Henriksen
Anthracycline chemotherapy causes dose-related cardiomyocyte injury and death leading to left ventricular dysfunction. Clinical heart failure may ensue in up to 5% of high-risk patients. Improved cancer survival together with better awareness of the late effects of cardiotoxicity has led to growing recognition of the need for surveillance of anthracycline-treated cancer survivors with early intervention to treat or prevent heart failure. The main mechanism of anthracycline cardiotoxicity is now thought to be through inhibition of topoisomerase 2β resulting in activation of cell death pathways and inhibition of mitochondrial biogenesis...
December 7, 2017: Heart: Official Journal of the British Cardiac Society
https://www.readbyqxmd.com/read/29216582/cellular-and-mitochondrial-determination-of-low-molecular-mass-organic-acids-by-lc-ms-ms
#15
Jessica Fiori, Elisa Amadesi, Flaminia Fanelli, Concetta Valentina Tropeano, Michela Rugolo, Roberto Gotti
A selective and sensitive method for the determination of low molecular mass organic acids (LMMOAs) in cell and mitochondrial extracts is presented. The analytical method consists in the separation by reversed phase liquid chromatography and detection with tandem mass spectrometry (LC-MS/MS) of the LMMOAs like malic, succinic, formic and citric acids. These acids are among the cellular intermediates of the tricarboxylic acid cycle (TCA), thus their quantitation can provide essential information about the catabolic and anabolic processes occurring in cells under physiological and pathological conditions...
November 29, 2017: Journal of Pharmaceutical and Biomedical Analysis
https://www.readbyqxmd.com/read/29215849/-study-of-mitochondrial-dysfunction-using-cytoplasmic-hybrid
#16
V V Sinyov, M A Sazonova, V P Karagodin, A I Ryzhkova, E V Galitsyna, A A Melnichenko, N A Demakova, T P Shkurat, I A Sobenin, A N Orekhov
Aim. This review article describes literature sources devoted to the investigation of mitochondrial dysfunction using cytoplasmic hybrids (cybrids). The presented studies were carried out on cultures of cybrid cell lines HL60, MOL T-4, A549, 143B, HeLa, Arpe-19, HEK-293, SH-SY5Y and NT2. According to the analysis of scientific world literature, some of the most promising models for studying mitochondrial dysfunction are cell cultures without mitochondria (rho0) and cytoplasmic hybrids containing one or several mutations of mitochondrial genome...
April 2017: Patologicheskaia Fiziologiia i èksperimental'naia Terapiia
https://www.readbyqxmd.com/read/29215066/pharmacological-inhibition-of-rev-erb-stimulates-differentiation-inhibits-turnover-and-reduces-fibrosis-in-dystrophic-muscle
#17
Ryan D Welch, Cyrielle Billon, Aurore-Cecile Valfort, Thomas P Burris, Colin A Flaveny
Duchenne muscular dystrophy (DMD) is a debilitating X-linked disorder that is fatal. DMD patients lack the expression of the structural protein dystrophin caused by mutations within the DMD gene. The absence of functional dystrophin protein results in excessive damage from normal muscle use due to the compromised structural integrity of the dystrophin associated glycoprotein complex. As a result, DMD patients exhibit ongoing cycles of muscle destruction and regeneration that promote inflammation, fibrosis, mitochondrial dysfunction, satellite cell (SC) exhaustion and loss of skeletal and cardiac muscle function...
December 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29214897/ss-31-peptide-enables-mitochondrial-targeting-drug-delivery-a-promising-therapeutic-alteration-to-prevent-hair-cell-damage-from-aminoglycosides
#18
Xiao Kuang, Shuang Zhou, Weiling Guo, Zhenjie Wang, Yanhui Sun, Hongzhuo Liu
Aminoglycoside-induced hearing loss stems from damage or loss of mechanosensory hair cells in the inner ear. Intrinsic mitochondrial cell death pathway plays a key role in that cellular dysfunction for which no proven effective therapies against oto-toxicities exist. Therefore, the aim of the present study was to develop a new mitochondrial targeting drug delivery system (DDS) that provided improved protection from gentamicin. Particularly, SS-31 peptide-conjugated geranylgeranylacetone (GGA) loaded poly(lactic-co-glycolic acid) (PLGA) nanoparticles were constructed successfully via emulsion-solvent evaporation method...
November 2017: Drug Delivery
https://www.readbyqxmd.com/read/29214868/sulfasalazine-induces-mitochondrial-dysfunction-and-renal-injury
#19
Hossein Niknahad, Reza Heidari, Roya Mohammadzadeh, Mohammad Mehdi Ommati, Forouzan Khodaei, Negar Azarpira, Narges Abdoli, Mahdi Zarei, Behnam Asadi, Maryam Rasti, Babak Shirazi Yeganeh, Vahid Taheri, Arastoo Saeedi, Asma Najibi
Sulfasalazine is a commonly used drug for the treatment of rheumatoid arthritis and inflammatory bowel disease. There are several cases of renal injury encompass sulfasalazine administration in humans. The mechanism of sulfasalazine adverse effects toward kidneys is obscure. Oxidative stress and its consequences seem to play a role in the sulfasalazine-induced renal injury. The current investigation was designed to investigate the effect of sulfasalazine on kidney mitochondria. Rats received sulfasalazine (400 and 600 mg/kg/day, oral) for 14 consecutive days...
November 2017: Renal Failure
https://www.readbyqxmd.com/read/29214717/bisphenol-a-is-an-exogenous-toxin-that-promotes-mitochondrial-injury-and-death-in-tubular-cells
#20
Enrique Bosch-Panadero, Sebastian Mas, Esther Civantos, Pedro Abaigar, Vanesa Camarero, Alberto Ruiz-Priego, Alberto Ortiz, Jesus Egido, Emilio González-Parra
BACKGROUND: Uremic toxins that accumulate in chronic kidney disease (CKD) contribute to CKD complications, such as CKD progression. Bisphenol A (BPA) is a ubiquitous environmental toxin, structurally related with p-cresol, that accumulates in CKD. Our aim was to characterize the nephrotoxic potential of BPA. Specifically, we addressed BPA toxicity over energy-demanding proximal tubular cells. METHODS: Cell death and oxidative stress were evaluated by flow cytometry and confocal microscopy in HK-2 human proximal tubular epithelial cells...
December 7, 2017: Environmental Toxicology
keyword
keyword
43370
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"