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mitochondria dysfunction

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https://www.readbyqxmd.com/read/29141199/disruption-of-mitochondrial-function-as-mechanism-for-anti-cancer-activity-of-a-novel-mitochondriotropic-menadione-derivative
#1
José Teixeira, Ricardo Amorim, Katia Santos, Pedro Soares, Sandipan Datta, Gino A Cortopassi, Teresa L Serafim, Vilma A Sardão, Jorge Garrido, Fernanda Borges, Paulo J Oliveira
Menadione, also known as vitamin K3, is a 2-methyl-1,4 naphthoquinone with a potent cytotoxic activity mainly resulting from its quinone redox-cycling with production of reactive oxygen species (ROS). Although increased ROS generation is considered a relevant mechanism in cancer cell death, it may not be sufficiently effective to kill cancer cells due to phenotypic adaptations. Therefore, combining ROS-generating agents with other molecules targeting important cancer cell phenotypes can be an effective therapeutic strategy...
November 12, 2017: Toxicology
https://www.readbyqxmd.com/read/29138968/mitochondrial-dysfunctions-contribute-to-energy-deficits-in-rodent-model-of-hepatic-encephalopathy
#2
Saurabh Dhanda, Aditya Sunkaria, Avishek Halder, Rajat Sandhir
Perturbations in the cerebral energy metabolism are anticipated to be an important factor by which ammonia may exert its toxic effects on the central nervous system. The present study was designed to investigate the role of impaired mitochondrial functions and cerebral energy metabolism in the development hepatic encephalopathy (HE) induced by of bile duct ligation (BDL). After four weeks of BDL, a significant increase in hepatic hydroxyproline and collagen content was observed which confirmed biliary fibrosis...
November 14, 2017: Metabolic Brain Disease
https://www.readbyqxmd.com/read/29137352/maternal-high-calorie-diet-induces-mitochondrial-dysfunction-and-senescence-phenotype-in-subcutaneous-fat-of-newborn-mice
#3
Daniele Lettieri-Barbato, Fabiana D'Angelo, Francesca Sciarretta, Giuseppe Tatulli, Flavia Tortolici, Maria Rosa Ciriolo, Katia Aquilano
Mitochondrial dysfunction, inflammation and senescence-like features are observed in adipose depots in aging and obesity. Herein, we evaluated how maternal high calorie diet (HCD) may impact on subcutaneous adipose tissue (sAT) of the newborn mice. Adult C57BL/6J mice were randomly divided in three groups: normal calorie diet (NCD), HCD and HCD supplemented with niacin 8 weeks before mating. Mothers and pups were then sacrificed and metabolic and molecular analyses were carried out on sAT. HCD induced mitochondria dysfunction in mothers without inflammation and senescence, whereas in pups we also revealed the occurrence of senescent phenotype...
October 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/29136781/andrographolide-sulfonate-improves-alzheimer-associated-phenotypes-and-mitochondrial-dysfunction-in-app-ps1-transgenic-mice
#4
Ji Geng, Wen Liu, Yuyun Xiong, Hongqun Ding, Chunhong Jiang, Xiaoling Yang, Xiang Li, Ahmed Elgehama, Yang Sun, Qiang Xu, Wenjie Guo, Jing Gao
Alzheimer's disease is a neurodegenerative disorder with Amyloid-β plaques onset, synaptic damage, and cognitive decline. Aβ deposits cause pathological events including oxidative stress, mitochondrial dysfunction, and neuron death. In this study, APPswe/PSENΔ9 double transgenic mice model was used to imitate Alzheimer's disease and the effect and possible mechanism of Andrographolide sulfonate were examined. Andrographolide sulfonate was given to the mice for 7 months before the onset of Aβ plaque. Spatial memory test showed that Andrographolide sulfonate treatment prevented cognitive decline...
November 8, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29135887/ischemia-reperfusion-injury-in-aged-livers-the-energy-metabolism-inflammatory-response-and-autophagy
#5
Chunyi Kan, Luisa Ungelenk, Amelie Lupp, Olaf Dirsch, Uta Dahmen
Due to the lack of adequate organs, the number of patients with end-stage liver diseases, acute liver failure or hepatic malignancies waiting for liver transplantation is constantly increasing. Accepting aged liver grafts is one of the strategies expanding the donor pool to ease the discrepancy between the growing demand and the limited supply of donor organs. However, recipients of organs from old donors may show an increased post-transplantation morbidity and mortality due to enhanced ischemia reperfusion injury...
November 11, 2017: Transplantation
https://www.readbyqxmd.com/read/29133339/decreased-ceramide-underlies-mitochondrial-dysfunction-in-charcot-marie-tooth-2f
#6
Nicholas U Schwartz, Ryan W Linzer, Jean-Philip Truman, Mikhail Gurevich, Yusuf A Hannun, Can E Senkal, Lina M Obeid
Charcot-Marie-Tooth (CMT) disease is the most commonly inherited neurologic disorder, but its molecular mechanisms remain unclear. One variant of CMT, 2F, is characterized by mutations in heat shock protein 27 (Hsp27). As bioactive sphingolipids have been implicated in neurodegenerative diseases, we sought to determine if their dysregulation is involved in CMT. Here, we show that Hsp27 knockout mice demonstrated decreases in ceramide in peripheral nerve tissue and that the disease-associated Hsp27 S135F mutant demonstrated decreases in mitochondrial ceramide...
November 13, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29132816/deferiprone-inhibits-iron-overload-induced-tissue-factor-bearing-endothelial-microparticle-generation-by-inhibition-oxidative-stress-induced-mitochondrial-injury-and-apoptosis
#7
Shing Chan, Qizhou Lian, Mei-Pian Chen, Dan Jiang, Jolie T K Ho, Yiu-Fai Cheung, Godfrey C F Chan
Iron overload-induced cardiovascular toxicity is one of the most common causes of morbidity and mortality in beta-thalassemia major patients. We have previously shown that iron overload-induced systemic arterial changes characterized by endothelial dysfunction are associated with increased endothelial microparticle (EMP) release. In this study, we further demonstrate how EMP release is associated with iron-induced mitochondrial injury and apoptosis of endothelial cells. Iron increased the production of reactive oxygen species (ROS) and calcium influx into mitochondria [Ca(2+)]m...
November 10, 2017: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29132140/mitochondria-targeted-peptide-attenuates-mitochondrial-dysfunction-controls-inflammation-and-protects-against-spinal-cord-injury-induced-lung-injury
#8
Liu-Long Zhu, Mao-Qiang Li, Fan He, Shao-Bo Zhou, Wu Jiang
BACKGROUND/AIMS: Spinal cord injury (SCI) is a common and devastating disease, which results in systemic inflammatory response syndrome and secondary lung injury. Mitochondrial dysfunction and inflammation are closely related to lung injury in diverse disease models. No studies have demonstrated the effects of mitochondrial targeted peptide SS-31 in a mouse model of SCI-induced lung injury. METHODS: Immediately after injury, mice in the treatment groups received a daily, single-dose intraperitoneal injection of SS-31 and for the next 2 days...
November 13, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29130578/sirt3-deregulation-is-linked-to-mitochondrial-dysfunction-in-alzheimer-s-disease
#9
Junghee Lee, Yunha Kim, Tian Liu, Yu Jin Hwang, Seung Jae Hyeon, Hyeonjoo Im, Kyungeun Lee, Victor E Alvarez, Ann C McKee, Soo-Jong Um, Manwook Hur, Inhee Mook-Jung, Neil W Kowall, Hoon Ryu
Alzheimer's disease (AD) is the leading cause of dementia in the elderly. Despite decades of study, effective treatments for AD are lacking. Mitochondrial dysfunction has been closely linked to the pathogenesis of AD, but the relationship between mitochondrial pathology and neuronal damage is poorly understood. Sirtuins (SIRT, silent mating type information regulation 2 homolog in yeast) are NAD-dependent histone deacetylases involved in aging and longevity. The objective of this study was to investigate the relationship between SIRT3 and mitochondrial function and neuronal activity in AD...
November 11, 2017: Aging Cell
https://www.readbyqxmd.com/read/29129747/mitochondrial-sirt3-and-neurodegenerative-brain-disorders
#10
REVIEW
Anamika, Archita Khanna, Papia Acharjee, Arup Acharjee, Surendra Kumar Trigun
Sirtuins are highly conserved NAD(+) dependent class III histone deacetylases and catalyze deacetylation and ADP ribosylation of a number of non-histone proteins. Since, they require NAD(+) for their activity, the cellular level of Sirtuins represents redox status of the cells and thereby serves as bona fide metabolic stress sensors. Out of seven homologues of Sirtuins identified in mammals, SIRT3, 4 & 5 have been found to be localized and active in mitochondria. During recent past, clusters of protein substrates for SIRT3 have been identified in mitochondria and thereby advocating SIRT3 as the main mitochondrial Sirtuin which could be involved in protecting stress induced mitochondrial integrity and energy metabolism...
November 9, 2017: Journal of Chemical Neuroanatomy
https://www.readbyqxmd.com/read/29129736/role-of-d-galactose-induced-brain-aging-and-its-potential-used-for-therapeutic-interventions
#11
REVIEW
Thazin-Shwe, Wasana Pratchayasakul, Nipon Chattipakorn, Siriporn C Chattipakorn
Aging is a phenomenon that all living organisms inevitably face. Every year, 9.9million people, globally, suffer from dementia, an indicator of the aging brain. Brain aging is significantly associated with mitochondrial dysfunction. This is characterized by a decrease in the activity of respiratory chain enzymes and ATP production, and increased free radical generation, mitochondrial deoxyribonucleic acid (DNA) mutations, and impaired mitochondrial structures. To get a better understanding of aging and to prevent its effects on many organs, chronic systemic administration of D-galactose was used to artificially create brain senescence in animal models and established to be beneficial for studies of anti-aging therapeutic interventions...
November 9, 2017: Experimental Gerontology
https://www.readbyqxmd.com/read/29129702/fkbp8-protects-the-heart-from-hemodynamic-stress-by-preventing-the-accumulation-of-misfolded-proteins-and-endoplasmic-reticulum-associated-apoptosis-in-mice
#12
Tomofumi Misaka, Tomokazu Murakawa, Kazuhiko Nishida, Yosuke Omori, Manabu Taneike, Shigemiki Omiya, Chris Molenaar, Yoshihiro Uno, Osamu Yamaguchi, Junji Takeda, Ajay M Shah, Kinya Otsu
Protein quality control in cardiomyocytes is crucial to maintain cellular homeostasis. The accumulation of damaged organelles, such as mitochondria and misfolded proteins in the heart is associated with heart failure. During the process to identify novel mitochondria-specific autophagy (mitophagy) receptors, we found FK506-binding protein 8 (FKBP8), also known as FKBP38, shares similar structural characteristics with a yeast mitophagy receptor, autophagy-related 32 protein. However, knockdown of FKBP8 had no effect on mitophagy in HEK293 cells or H9c2 myocytes...
November 9, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29128369/inhibition-of-poly-adp-ribose-polymerase-1-alters-expression-of-mitochondria-related-genes-in-pc12-cells-relevance-to-mitochondrial-homeostasis-in-neurodegenerative-disorders
#13
Grzegorz A Czapski, Magdalena Cieślik, Przemysław L Wencel, Sylwia Wójtowicz, Robert P Strosznajder, Joanna B Strosznajder
Alzheimer's disease (AD) is characterized by the release of amyloid beta peptides (Aβ) in the form of monomers/oligomers which may lead to oxidative stress, mitochondria dysfunction, synaptic loss, neuroinflammation and, in consequence, to overactivation of poly(ADP-ribose) polymerase-1 (PARP-1). However, Aβ peptides are also released in the brain ischemia, traumatic injury and in inflammatory response. PARP-1 is suggested to be a promising target in therapy of neurodegenerative disorders. We investigated the impact of PARP-1 inhibition on transcription of mitochondria-related genes in PC12 cells...
November 8, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29127580/sigma-1-receptor-agonists-induce-oxidative-stress-in-mitochondria-and-enhance-complex-i-activity-in-physiological-condition-but-protect-against-pathological-oxidative-stress
#14
Nino Goguadze, Elene Zhuravliova, Didier Morin, Davit Mikeladze, Tangui Maurice
The sigma1 receptor (σ1R) is a chaperone protein residing at mitochondria-associated endoplasmic reticulum (ER) membranes (MAMs), where it modulates Ca(2+) exchange between the ER and mitochondria by interacting with inositol-1,4,5 trisphosphate receptors (IP3Rs). The σ1R is highly expressed in the central nervous system and its activation stimulates neuromodulation and neuroprotection, for instance in Alzheimer's disease (AD) models in vitro and in vivo. σ1R effects on mitochondria pathophysiology and the downstream signaling are still not fully understood...
November 10, 2017: Neurotoxicity Research
https://www.readbyqxmd.com/read/29127319/mitochondrial-gene-polymorphism-is-associated-with-gut-microbial-communities-in-mice
#15
Misa Hirose, Axel Künstner, Paul Schilf, Annika Sünderhauf, Jan Rupp, Olaf Jöhren, Markus Schwaninger, Christian Sina, John F Baines, Saleh M Ibrahim
Gut microbial communities are key mediators of health and disease and have the capacity to drive the pathogenesis of diverse complex diseases including metabolic and chronic inflammatory diseases as well as aging. Host genetics is also a major determinant of disease phenotypes, whereby two different genomes play a role, the nuclear (nDNA)- and mitochondrial genome (mtDNA). We investigated the impact of mutations in mtDNA on the gut microbiota using conplastic mouse strains exhibiting distinct mutations in their mtDNA on an identical nDNA...
November 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29127192/lipotoxic-very-long-chain-ceramides-cause-mitochondrial-dysfunction-oxidative-stress-and-cell-death-in-cardiomyocytes
#16
Brittany A Law, Xianghai Liao, Kelsey S Moore, Abigail Southard, Patrick Roddy, Ruiping Ji, Zdzislaw Sculz, Ala Bielawska, P Christian Schulze, L Ashley Cowart
Accumulating data support a role for bioactive lipids as mediators of lipotixicity in cardiomyocytes. One class of these, the ceramides, constitutes a family of molecules that differ in structure and are synthesized by distinct enzymes, ceramide synthase (CerS)1-CerS6. Data support that specific ceramides and the enzymes that catalyze their formation play distinct roles in cell function. In a mouse model of diabetic cardiomyopathy, sphingolipid profiling revealed increases in not only the CerS5-derived ceramides but also in very long chain (VLC) ceramides derived from CerS2...
November 10, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29127187/apobec2-deficiency-causes-mitochondrial-defects-and-mitophagy-in-skeletal-muscle
#17
Yusuke Sato, Hideaki Ohtsubo, Naohiro Nihei, Takane Kaneko, Yoriko Sato, Shin-Ichi Adachi, Shinji Kondo, Mako Nakamura, Wataru Mizunoya, Hiroshi Iida, Ryuichi Tatsumi, Cristina Rada, Fumiaki Yoshizawa
Apobec2 is a member of the activation-induced deaminase/apolipoprotein B mRNA editing enzyme catalytic polypeptide cytidine deaminase family expressed in differentiated skeletal and cardiac muscle. We previously reported that Apobec2 deficiency in mice leads to a shift in muscle fiber type, myopathy, and diminished muscle mass. However, the mechanisms of myopathy caused by Apobec2 deficiency and its physiologic functions are unclear. Here we show that, although Apobec2 localizes to the sarcomeric Z-lines in mouse tissue and cultured myotubes, the sarcomeric structure is not affected in Apobec2-deficient muscle...
November 10, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/29125827/early-cerebellar-deficits-in-mitochondrial-biogenesis-and-respiratory-chain-complexes-in-the-kiko-mouse-model-of-friedreich-ataxia
#18
Hong Lin, Jordi Magrane, Amy Rattelle, Anna Stepanova, Alexander Galkin, Elisia M Clark, Yi Na Dong, Sarah M Halawani, David R Lynch
Friedreich ataxia (FRDA), the most common recessive inherited ataxia, results from deficiency of frataxin, a small mitochondrial protein crucial for iron-sulphur cluster formation and ATP production. Frataxin deficiency is associated with mitochondrial dysfunction in FRDA patients and animal models; however, early mitochondrial pathology in FRDA cerebellum remains elusive. Using frataxin knock-in/knockout (KIKO) mice and KIKO mice carrying the mitoDendra transgene, we show early cerebellar deficits in mitochondrial biogenesis and respiratory chain complexes in this FRDA model...
November 1, 2017: Disease Models & Mechanisms
https://www.readbyqxmd.com/read/29125070/circulating-mitochondrial-dna-at-the-crossroads-of-mitochondrial-dysfunction-and-inflammation-during-aging-and-muscle-wasting-disorders
#19
Anna Picca, Angela Maria Serena Lezza, Christiaan Leeuwenburgh, Vito Pesce, Riccardo Calvani, Maurizio Bossola, Ester Manes-Gravina, Francesco Landi, Roberto Bernabei, Emanuele Marzetti
Mitochondrial structural and functional integrity is maintained through the coordination of several processes (e.g., biogenesis, dynamics, mitophagy), collectively referred to as mitochondrial quality control. Dysfunctional mitochondrial quality control and inflammation are hallmarks of aging and are involved in the pathogenesis of muscle wasting disorders, including sarcopenia and cachexia. One of the consequences of failing mitochondrial quality control is the release of mitochondria-derived damage-associated molecular patterns...
November 10, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/29123128/pink1-mediated-phosphorylation-of-letm1-regulates-mitochondrial-calcium-transport-and-protects-neurons-against-mitochondrial-stress
#20
En Huang, Dianbo Qu, Tianwen Huang, Nicoletta Rizzi, Wassamon Boonying, Dorothy Krolak, Paolo Ciana, John Woulfe, Christine Klein, Ruth S Slack, Daniel Figeys, David S Park
Mutations in PTEN-induced kinase 1 (PINK1) result in a recessive familial form of Parkinson's disease (PD). PINK1 loss is associated with mitochondrial Ca(2+) mishandling, mitochondrial dysfunction, as well as increased neuronal vulnerability. Here we demonstrate that PINK1 directly interacts with and phosphorylates LETM1 at Thr192 in vitro. Phosphorylated LETM1 or the phospho-mimetic LETM1-T192E increase calcium release in artificial liposomes and facilitates calcium transport in intact mitochondria. Expression of LETM1-T192E but not LETM1-wild type (WT) rescues mitochondrial calcium mishandling in PINK1-deficient neurons...
November 9, 2017: Nature Communications
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