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https://www.readbyqxmd.com/read/29786070/selective-elimination-of-senescent-cells-by-mitochondrial-targeting-is-regulated-by-ant2
#1
Sona Hubackova, Eliska Davidova, Katerina Rohlenova, Jan Stursa, Lukas Werner, Ladislav Andera, LanFeng Dong, Mikkel G Terp, Zdenek Hodny, Henrik J Ditzel, Jakub Rohlena, Jiri Neuzil
Cellular senescence is a form of cell cycle arrest that limits the proliferative potential of cells, including tumour cells. However, inability of immune cells to subsequently eliminate senescent cells from the organism may lead to tissue damage, inflammation, enhanced carcinogenesis and development of age-related diseases. We found that the anticancer agent mitochondria-targeted tamoxifen (MitoTam), unlike conventional anticancer agents, kills cancer cells without inducing senescence in vitro and in vivo. Surprisingly, it also selectively eliminates both malignant and non-cancerous senescent cells...
May 21, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29784660/interleukin-6-reduces-%C3%AE-cell-oxidative-stress-by-linking-autophagy-with-the-antioxidant-response
#2
Michelle R Marasco, Abass M Conteh, Christopher A Reissaus, John E Cupit V, Evan M Appleman, Raghavendra G Mirmira, Amelia K Linnemann
Production of reactive oxygen species (ROS) is a key instigator of β-cell dysfunction in diabetes. The pleiotropic cytokine IL-6 has previously been linked to β-cell autophagy but has not been studied in the context of β-cell antioxidant response. We used a combination of animal models of diabetes and analysis of cultured human islets and rodent β-cells to study how IL-6 influences antioxidant response. We show that IL-6 couples autophagy to antioxidant response to reduce β-cell and human islet ROS. β cell-specific loss of IL-6 signaling in vivo renders mice more susceptible to oxidative damage and cell death by the selective β-cell toxins streptozotocin and alloxan...
May 21, 2018: Diabetes
https://www.readbyqxmd.com/read/29783748/neuronal-dysfunction-associated-with-cholesterol-deregulation
#3
Annalisa Marcuzzi, Claudia Loganes, Erica Valencic, Elisa Piscianz, Lorenzo Monasta, Sabrine Bilel, Roberta Bortul, Claudio Celeghini, Marina Zweyer, Alberto Tommasini
Cholesterol metabolism is crucial for cells and, in particular, its biosynthesis in the central nervous system occurs in situ, and its deregulation involves morphological changes that cause functional variations and trigger programmed cell death. The pathogenesis of rare diseases, such as Mevalonate Kinase Deficiency or Smith⁻Lemli⁻Opitz Syndrome, arises due to enzymatic defects in the cholesterol metabolic pathways, resulting in a shortage of downstream products. The most severe clinical manifestations of these diseases appear as neurological defects...
May 19, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29781318/hypochlorite-modified-albumins-promote-cell-death-in-the-tubule-interstitium-in-rats-via-mitochondrial-damage-in-obstructive-nephropathy-and-the-protective-effects-of-antioxidant-peptides
#4
Zong-Rui Liu, Si-Qi Chen, Yao-Wei Zou, Xiao-Yu Wu, Hong-Ying Li, Xiao-Qiao Wang, Yue Shi, Hong-Xin Niu
A major feature of the injury sustained by the kidney during obstructive nephropathy is a profound induction of apoptosis in the tubular epithelium. In this study, we explored the central roles of mitochondria and the mechanism of the protective effect of the mitochondrial targeted peptides in tubular cell apoptosis and interstitial fibrosis during obstructive nephropathy. Unilateral ureter obstruction (UUO) was performed on rats, and the animals were randomly assigned to intravenous treatment with normal saline, rat serum albumin (RSA), or HOCl-rat serum albumin (HOCl-RSA) in the presence or absence of SS-31...
May 2018: Free Radical Research
https://www.readbyqxmd.com/read/29781122/protective-effects-of-endothelial-progenitor-cell-derived-extracellular-mitochondria-in-brain-endothelium
#5
Kazuhide Hayakawa, Su Jing Chan, Emiri T Mandeville, Ji Hyun Park, Morgan Bruzzese, Joan Montaner, Ken Arai, Anna Rosell, Eng H Lo
Endothelial progenitor cells (EPCs) have been pursued as a potential cellular therapy for stroke and central nervous system injury. However, their underlying mechanisms remain to be fully defined. Recent experimental studies suggest that mitochondria may be released and transferred between cells. In this proof-of-concept study, we asked whether beneficial effects of EPCs may partly involve a mitochondrial phenomenon as well. First, EPC-derived conditioned medium was collected and divided into supernatant and particle fractions after centrifugation...
May 21, 2018: Stem Cells
https://www.readbyqxmd.com/read/29779213/differential-toxicity-of-tdp-43-isoforms-depends-on-their-sub-mitochondrial-localization-in-neuronal-cells
#6
Illari Salvatori, Alberto Ferri, Silvia Scaricamazza, Ilaria Giovannelli, Alessia Serrano, Simona Rossi, Nadia D'Ambrosi, Mauro Cozzolino, Andrea Di Giulio, Sandra Moreno, Cristiana Valle, Maria Teresa Carrì
TAR DNA binding protein 43 (TDP-43) is an RNA binding protein and a major component of protein aggregates found in Amyotrophic Lateral Sclerosis and several other neurodegenerative diseases. TDP-43 exists as a full length protein and as two shorter forms of 25 and 35 kDa. Full length mutant TDP-43s found in ALS patients re-localize from the nucleus to the cytoplasm and in part to mitochondria, where they exert a toxic role associated with neurodegeneration. However, induction of mitochondrial damage by TDP-43 fragments is yet to be clarified...
May 20, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29778900/hereditary-sensory-neuropathy-type-1-associated-deoxysphingolipids-cause-neurotoxicity-acute-calcium-handling-abnormalities-and-mitochondrial-dysfunction-in-vitro
#7
Emma R Wilson, Umaiyal Kugathasan, Andrey Y Abramov, Alex J Clark, David L H Bennett, Mary M Reilly, Linda Greensmith, Bernadett Kalmar
Hereditary sensory neuropathy type 1 (HSN-1) is a peripheral neuropathy most frequently caused by mutations in the SPTLC1 or SPTLC2 genes, which code for two subunits of the enzyme serine palmitoyltransferase (SPT). SPT catalyzes the first step of de novo sphingolipid synthesis. Mutations in SPT result in a change in enzyme substrate specificity, which causes the production of atypical deoxysphinganine and deoxymethylsphinganine, rather than the normal enzyme product, sphinganine. Levels of these abnormal compounds are elevated in blood of HSN-1 patients and this is thought to cause the peripheral motor and sensory nerve damage that is characteristic of the disease, by a largely unresolved mechanism...
May 17, 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29778462/altered-mitochondrial-acetylation-profiles-in-a-kainic-acid-model-of-temporal-lobe-epilepsy
#8
Lindsey B Gano, Li-Ping Liang, Kristen Ryan, Cole R Michel, Joe Gomez, Athanassios Vassilopoulos, Nichole Reisdorph, Kristofer S Fritz, Manisha Patel
Impaired bioenergetics and oxidative damage in the mitochondria are implicated in the etiology of temporal lobe epilepsy, and hyperacetylation of mitochondrial proteins has recently emerged as a critical negative regulator of mitochondrial functions. However, the roles of mitochondrial acetylation and activity of the primary mitochondrial deacetylase, SIRT3, have not been explored in acquired epilepsy. We investigated changes in mitochondrial acetylation and SIRT3 activity in the development of chronic epilepsy in the kainic acid rat model of TLE...
May 17, 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/29777685/thiamine-preserves-mitochondrial-function-in-a-rat-model-of-traumatic-brain-injury-preventing-inactivation-of-the-2-oxoglutarate-dehydrogenase-complex
#9
Garik V Mkrtchyan, Muammer Üçal, Andrea Müllebner, Sergiu Dumitrescu, Martina Kames, Rudolf Moldzio, Marek Molcanyi, Samuel Schaefer, Adelheid Weidinger, Ute Schaefer, Juergen Hescheler, Johanna Catharina Duvigneau, Heinz Redl, Victoria I Bunik, Andrey V Kozlov
BACKGROUND AND PURPOSE: Based on the fact that traumatic brain injury is associated with mitochondrial dysfunction we aimed at localization of mitochondrial defect and attempted to correct it by thiamine. EXPERIMENTAL APPROACH: Interventional controlled experimental animal study was used. Adult male Sprague-Dawley rats were subjected to lateral fluid percussion traumatic brain injury. Thiamine was administered 1 h prior to trauma; cortex was extracted for analysis 4 h and 3 d after trauma...
May 16, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29777261/mitochondrial-quality-control-in-amd-does-mitophagy-play-a-pivotal-role
#10
REVIEW
Juha M T Hyttinen, Johanna Viiri, Kai Kaarniranta, Janusz Błasiak
Age-related macular degeneration (AMD) is the predominant cause of visual loss in old people in the developed world, whose incidence is increasing. This disease is caused by the decrease in macular function, due to the degeneration of retinal pigment epithelium (RPE) cells. The aged retina is characterised by increased levels of reactive oxygen species (ROS), impaired autophagy, and DNA damage that are linked to AMD pathogenesis. Mitophagy, a mitochondria-specific type of autophagy, is an essential part of mitochondrial quality control, the collective mechanism responsible for this organelle's homeostasis...
May 18, 2018: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/29775411/humanin-analogue-hng-enhances-the-protective-effect-of-dexrazoxane-against-doxorubicin-induced-cardiotoxicity
#11
YanHe Lue, Chen Gao, Ronald S Swerdloff, James Hoang, Rozeta Avetisyan, Yue Jia, Meng Rao, Shuxun Ren, Vince Atienza, Junyi Yu, Yie Zhang, Mengping Chen, Yang Song, Yibin Wang, Christina Wang
The chemotherapeutic effect of Doxorubicin (Dox) is limited by cumulative dose-dependent cardiotoxicity in cancer survivors. Dexrazoxane (DRZ) is approved to prevent Dox-induced cardiotoxicity. Humanin and its synthetic analog HNG have cytoprotective effect on the heart. To investigate the cardioprotective efficacy of HNG alone or in combination with DRZ against Dox-induced cardiotoxicity, eighty adult male mice were randomly divided into 8 groups to receive the following treatments via intraperitoneal injection: saline daily; HNG (5mg/kg) daily; DRZ (60mg/kg) weekly; Dox (3mg/kg) weekly; DRZ+HNG, Dox+HNG; Dox+DRZ and Dox+HNG+DRZ...
May 18, 2018: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29772718/ectromelia-virus-affects-mitochondrial-network-morphology-distribution-and-physiology-in-murine-fibroblasts-and-macrophage-cell-line
#12
Karolina P Gregorczyk, Zbigniew Wyżewski, Joanna Szczepanowska, Felix N Toka, Matylda B Mielcarska, Magdalena Bossowska-Nowicka, Małgorzata Gieryńska, Anna Boratyńska-Jasińska, Justyna Struzik, Marek G Niemiałtowski, Lidia Szulc-Dąbrowska
Mitochondria are multifunctional organelles that participate in numerous processes in response to viral infection, but they are also a target for viruses. The aim of this study was to define subcellular events leading to alterations in mitochondrial morphology and function during infection with ectromelia virus (ECTV). We used two different cell lines and a combination of immunofluorescence techniques, confocal and electron microscopy, and flow cytometry to address subcellular changes following infection. Early in infection of L929 fibroblasts and RAW 264...
May 16, 2018: Viruses
https://www.readbyqxmd.com/read/29770896/mitochondrial-morphology-and-function-impaired-by-dimethyl-sulfoxide-and-dimethyl-formamide
#13
Long Ma, Jia-Xin Dong, Wen-Rong Fu, Xue-Yi Li, Jing Chen, Yi Liu
In this work, the effects of two non-ionic, non-hydroxyl organic solvents, dimethyl sulfoxide (DMSO) and dimethyl formamide (DMF) on the morphology and function of isolated rat hepatic mitochondria were investigated and compared. Mitochondrial ultrastructures impaired by DMSO and DMF were clearly observed by transmission electron microscopy. Spectroscopic and polarographic results demonstrated that organic solvents induced mitochondrial swelling, enhanced the permeation to H+ /K+ , collapsed the potential inner mitochondrial membrane (IMM), and increased the IMM fluidity...
May 17, 2018: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/29767769/regulation-of-chlorophagy-during-photoinhibition-and-senescence-lessons-from-mitophagy
#14
Sakuya Nakamura, Masanori Izumi
Light energy is essential for photosynthetic energy production and plant growth. Chloroplasts in green tissues convert energy from sunlight into chemical energy via the electron transport chain. When the level of light energy exceeds the capacity of the photosynthetic apparatus, chloroplasts undergo a process known as photoinhibition. Since photoinhibition leads to the overaccumulation of reactive oxygen species (ROS) and the spreading of cell death, plants have developed multiple systems to protect chloroplasts from strong light...
May 14, 2018: Plant & Cell Physiology
https://www.readbyqxmd.com/read/29767280/carnosine-and-histidine-supplementation-blunt-lead-induced-reproductive-toxicity-through-antioxidative-and-mitochondria-dependent-mechanisms
#15
Mohammad Mehdi Ommati, Akram Jamshidzadeh, Reza Heidari, Zilong Sun, Mohammad Javad Zamiri, Forouzan Khodaei, Saeed Mousapour, Fatemeh Ahmadi, Nafiseh Javanmard, Babak Shirazi Yeganeh
Lead (Pb)-induced reproductive toxicity is a well-characterized adverse effect associated with this heavy metal. It has been found that Pb exposure is associated with altered spermatogenesis, increased testicular degeneration, and pathological sperm alterations. On the other hand, it has been reported that Pb-induced reproductive toxicity is associated with increased reactive oxygen species (ROS) formation and diminished antioxidant capacity in the reproductive system. Hence, administration of antioxidants as protective agents might be of value against Pb-induced reproductive toxicity...
May 16, 2018: Biological Trace Element Research
https://www.readbyqxmd.com/read/29765325/mequindox-induced-kidney-toxicity-is-associated-with-oxidative-stress-and-apoptosis-in-the-mouse
#16
Qianying Liu, Zhixin Lei, Jingchao Guo, Aimei Liu, Qirong Lu, Zainab Fatima, Haseeb Khaliq, Muhammad A B Shabbir, Muhammad Kashif Maan, Qinghua Wu, Menghong Dai, Xu Wang, Yuanhu Pan, Zonghui Yuan
Mequindox (MEQ), belonging to quinoxaline-di- N -oxides (QdNOs), is a synthetic antimicrobial agent widely used in China. Previous studies found that the kidney was one of the main toxic target organs of the QdNOs. However, the mechanisms underlying the kidney toxicity caused by QdNOs in vivo still remains unclear. The present study aimed to explore the molecular mechanism of kidney toxicity in mice after chronic exposure to MEQ. MEQ led to the oxidative stress, apoptosis, and mitochondrial damage in the kidney of mice...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29764717/mitochondrial-damage-and-cytoskeleton-reorganization-in-human-dermal-fibroblasts-exposed-to-artificial-visible-light-similar-to-screen-emitted-light
#17
Adeline Rascalou, Jérôme Lamartine, Pauline Poydenot, Frédéric Demarne, Nicolas Bechetoille
BACKGROUND: Artificial visible light is everywhere in modern life. Social communication confronts us with screens of all kinds, and their use is on the rise. We are therefore increasingly exposed to artificial visible light, the effects of which on skin are poorly known. OBJECTIVE: The purpose of this study was to model the artificial visible light emitted by electronic devices and assess its effect on normal human fibroblasts. METHODS: The spectral irradiance emitted by electronic devices was optically measured and equipment was developed to accurately reproduce such artificial visible light...
May 5, 2018: Journal of Dermatological Science
https://www.readbyqxmd.com/read/29762502/molecular-mechanisms-of-apoptosis-in-heparg-cell-line-induced-by-polyphyllin-vi-via-the-fas-death-pathway-and-mitochondrial-dependent-pathway
#18
Yi Liu, Xiaoxv Dong, Wenping Wang, Longtai You, Xingbin Yin, Chunjing Yang, Na Sai, Xin Leng, Jian Ni
Polyphyllin VI, which is an active saponin, is mainly isolated from traditional medicinal plant Paris polyphylla , which causes liver damage in rats. In the present study, we aimed to explore the potential cytotoxicity of polyphyllin VI on the growth of HepaRG cells and to determine the molecular mechanism. The results revealed that polyphyllin VI changed cell morphology and induced apoptosis in HepaRG cells. Flow cytometric assay displayed that polyphyllin VI promoted the generation of reactive oxygen species (ROS), depolarized the mitochondrial membrane potential (MMP), and induced S phase cell cycle arrest by decreasing the expression of cyclin A2 and CDK2, while significantly increasing the expression of p21 protein...
May 15, 2018: Toxins
https://www.readbyqxmd.com/read/29761302/cftr-prevents-neuronal-apoptosis-following-cerebral-ischemia-reperfusion-via-regulating-mitochondrial-oxidative-stress
#19
Ya-Ping Zhang, Yong Zhang, Zhi-Bin Xiao, Yan-Bo Zhang, Jing Zhang, Zhi-Qiang Li, Yao-Bin Zhu
The cystic fibrosis transmembrane conductance regulator (CFTR) is linked to cell apoptosis and abundantly expressed in brain tissue. Mitochondrial oxidative stress plays a key role in activating apoptotic pathway following cerebral ischemia reperfusion (IR) injury. Reduced glutathione (GSH) is exclusively synthesized in cytosol but distributed in mitochondria. In the present study, we investigated whether CFTR affected mitochondrial oxidative stress via regulating GSH and thereby protected neurons against apoptosis following cerebral IR...
May 14, 2018: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://www.readbyqxmd.com/read/29760744/mst1-regulates-post-infarction-cardiac-injury-through-the-jnk-drp1-mitochondrial-fission-pathway
#20
Xisong Wang, Qing Song
Background: Post-infarction cardiac injury is closely associated with cardiac remodeling and heart dysfunction. Mammalian STE20-like kinase 1 (Mst1), a regulator of cellular apoptosis, is involved in cardiac remodeling in post-infarction heart, but the mechanisms remain poorly defined. We aimed to explore the role of Mst1 in regulating chronic post-infarction cardiac injury, with a focus on mitochondrial homoeostasis. Methods: Wild-type (WT) and Mst1-knockout mice were as the cardiac myocardial infarction model...
2018: Cellular & Molecular Biology Letters
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