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Mitochondrial dysfunction

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https://www.readbyqxmd.com/read/29036828/mitochondria-and-mitochondrial-cascades-in-alzheimer-s-disease
#1
Russell H Swerdlow
Decades of research indicate mitochondria from Alzheimer's disease (AD) patients differ from those of non-AD individuals. Initial studies revealed structural differences, and subsequent studies showed functional deficits. Observations of structure and function changes prompted investigators to consider the consequences, significance, and causes of AD-related mitochondrial dysfunction. Currently, extensive research argues mitochondria may mediate, drive, or contribute to a variety of AD pathologies. The perceived significance of these mitochondrial changes continues to grow, and many currently believe AD mitochondrial dysfunction represents a reasonable therapeutic target...
October 7, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/29036556/deficit-in-pink1-parkin-mediated-mitochondrial-autophagy-at-late-stages-of-dystrophic-cardiomyopathy
#2
Chifei Kang, Myriam A Badr, Viktoriia Kyrychenko, Eeva-Liisa Eskelinen, Natalia Shirokova
Aims: Duchenne Muscular Dystrophy (DMD) is an inherited devastating muscle disease with severe and often lethal cardiac complications. Emerging evidence suggests that the evolution of the pathology in DMD is accompanied by the accumulation of mitochondria with defective structure and function. Here we investigate whether defects in the housekeeping autophagic pathway contribute to mitochondrial and metabolic dysfunctions in dystrophic cardiomyopathy. Methods and results: We employed various biochemical and imaging techniques to assess mitochondrial structure and function as well as to evaluate autophagy, and specific mitochondrial autophagy (mitophagy), in hearts of mdx mice, an animal model of DMD...
October 5, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/29036219/correction-role-of-mitochondrial-dna-damage-and-dysfunction-in-veterans-with-gulf-war-illness
#3
Yang Chen, Joel N Meyer, Helene Z Hill, Gudrun Lange, Michael R Condon, Jacquelyn C Klein, Duncan Ndirangu, Michael J Falvo
[This corrects the article DOI: 10.1371/journal.pone.0184832.].
2017: PloS One
https://www.readbyqxmd.com/read/29035972/hyperammonemia-and-proteostasis-in-cirrhosis
#4
Srinivasan Dasarathy, Maria Hatzoglou
PURPOSE OF REVIEW: Skeletal muscle loss or sarcopenia is a frequent complication of cirrhosis that adversely affects clinical outcomes. As skeletal muscle is the largest store of proteins in the body, proteostasis or protein homeostasis is required for maintenance of muscle mass. This review will focus on disordered skeletal muscle proteostasis in liver disease. RECENT FINDINGS: Increased skeletal muscle uptake of ammonia initiates responses that result in disordered proteostasis including impaired protein synthesis and increased autophagy...
October 14, 2017: Current Opinion in Clinical Nutrition and Metabolic Care
https://www.readbyqxmd.com/read/29035693/mms19-localizes-to-mitochondria-and-protects-the-mitochondrial-genome-from-oxidative-damage
#5
Rui Wu, Qunsong Tan, Kaifeng Niu, Yuqi Zhu, Di Wei, Yongliang Zhao, Hongbo Fang
MMS19 localizes to cytoplasmic and nuclear compartments involving in transcription and nucleotide excision repair (NER). However, whether or not MMS19 localizes to mitochondria where it plays a role in maintaining mitochondrial genome stability remains elusive. In this study, we provide the first evidence that MMS19 is localized in the inner membrane of mitochondria and participates in mtDNA oxidative damage repair. MMS19 knockdown led to mitochondrial dysfunctions including decreased mtDNA copy number, diminished mtDNA repair capacity and elevated level of mtDNA common deletion after oxidative stress...
October 16, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29035377/nme4-nucleoside-diphosphate-kinase-d-in-cardiolipin-signaling-and-mitophagy
#6
Uwe Schlattner, Malgorzata Tokarska-Schlattner, Richard M Epand, Mathieu Boissan, Marie-Lise Lacombe, Valerian E Kagan
Mitophagy is an emerging paradigm for mitochondrial quality control and cell homeostasis. Dysregulation of mitophagy can lead to human pathologies such as neurodegenerative disorders and contributes to the aging process. Complex protein signaling cascades have been described that regulate mitophagy. We have identified a novel lipid signaling pathway that involves the phospholipid cardiolipin (CL). CL is synthesized and normally confined at the inner mitochondrial membrane. However, upon a mitophagic trigger, ie, collapse of the inner membrane potential, CL is rapidly externalized to the mitochondrial surface with the assistance of the hexameric nucleoside diphosphate kinase D (NME4, NDPK-D, or NM23-H4)...
October 16, 2017: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/29034965/role-of-serum-albumin-as-a-nanoparticulate-carrier-for-nose-to-brain-delivery-of-r-flurbiprofen-implications-for-the-treatment-of-alzheimer-s-disease
#7
Ling Rong Wong, Paul C Ho
OBJECTIVES: R-flurbiprofen (R-FP) was found to offer neuroprotective effects by inhibiting mitochondrial calcium overload induced by β-amyloid peptide toxicity in Alzheimer's disease (AD). However, poor brain penetration after oral administration posed a challenge to its further development for AD treatment. In this study, we investigated the potential of serum albumin as nanoparticulate carriers for nose-to-brain delivery of R-FP to improve its brain accumulation. METHODS: Mice were subjected to three treatment groups: (1) intranasal R-FP solution, (2) oral R-FP solution and (3) intranasal R-FP albumin nanoparticles...
October 16, 2017: Journal of Pharmacy and Pharmacology
https://www.readbyqxmd.com/read/29034472/protective-effects-of-curcumin-against-aflatoxicosis-a-comprehensive-review
#8
REVIEW
Mohammad Mohajeri, Behzad Behnam, Arrigo F G Cicero, Amirhossein Sahebkar
Aflatoxicosis is a deleterious medical condition that results from aflatoxins (AFs) or ochratoxins (OTs). Contamination with these toxins exerts detrimental effects on the liver, kidneys, reproductive organs, and also on immunological and cardiovascular systems. Aflatoxicosis is closely associated with overproduction of reactive oxygen species (ROS) as key contributors to oxidative and nitrosative stress responses, and subsequent damages to lipids, proteins, RNA, and DNA. The main target organ for AF toxicity is the liver, where DNA adducts, degranulation of endoplasmic reticulum, increased hepatic lipid peroxide, GSH depletion, mitochondrial dysfunction, and reduction of enzymatic and non-enzymatic antioxidants are manifestations of aflatoxicosis...
October 16, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29033794/dihydroartemisinin-exerts-anti-tumor-activity-by-inducing-mitochondrion-and-endoplasmic-reticulum-apoptosis-and-autophagic-cell-death-in-human-glioblastoma-cells
#9
Chengbin Qu, Jun Ma, Xiaobai Liu, Yixue Xue, Jian Zheng, Libo Liu, Jing Liu, Zhen Li, Lei Zhang, Yunhui Liu
Glioblastoma (GBM) is the most advanced and aggressive form of gliomas. Dihydroartemisinin (DHA) has been shown to exhibit anti-tumor activity in various cancer cells. However, the effect and molecular mechanisms underlying its anti-tumor activity in human GBM cells remain to be elucidated. Our results proved that DHA treatment significantly reduced cell viability in a dose- and time-dependent manner by CCK-8 assay. Further investigation identified that the cell viability was rescued by pretreatment either with Z-VAD-FMK, 3-methyladenine (3-MA) or in combination...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29032504/resistance-exercise-improves-cardiac-function-and-mitochondrial-efficiency-in-diabetic-rat-hearts
#10
Tae Hee Ko, Jubert C Marquez, Hyoung Kyu Kim, Seung Hun Jeong, SungRyul Lee, Jae Boum Youm, In Sung Song, Dae Yun Seo, Hye Jin Kim, Du Nam Won, Kyoung Im Cho, Mun Gi Choi, Byoung Doo Rhee, Kyung Soo Ko, Nari Kim, Jong Chul Won, Jin Han
Metabolic disturbance and mitochondrial dysfunction are a hallmark of diabetic cardiomyopathy (DC). Resistance exercise (RE) not only enhances the condition of healthy individuals but could also improve the status of those with disease. However, the beneficial effects of RE in the prevention of DC and mitochondrial dysfunction are uncertain. Therefore, this study investigated whether RE attenuates DC by improving mitochondrial function using an in vivo rat model of diabetes. Fourteen Otsuka Long-Evans Tokushima Fatty rats were assigned to sedentary control (SC, n = 7) and RE (n = 7) groups at 28 weeks of age...
October 14, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/29032222/molecular-mechanisms-of-nickel-induced-neurotoxicity-and-chemoprevention
#11
REVIEW
Xin Song, Samuel Selorm Fiatikenston, Lu Kong, Jinshun Zhao
Nickel (Ni) is widely used in many industrial sectors such as alloy, welding, printing inks, electrical and electronics industries. Excessive environmental or occupational exposure to Ni may result in tumor, contact dermatitis, as well as damages to the nervous system. In recent years, more and more research has demonstrated that Ni induced nerve damages are related to mitochondrial dysfunction. In this paper, we try to characterize Ni induced neurotoxicity as well as the underlying mechanisms, and how to find new drugs for chemoprevention, by reviewing chemicals with neuroprotective effects on Ni induced neurotoxicity...
October 11, 2017: Toxicology
https://www.readbyqxmd.com/read/29031832/initial-brain-aging-heterogeneity-of-mitochondrial-size-is-associated-with-decline-in-complex-i-linked-respiration-in-cortex-and-hippocampus
#12
Kirsten Thomsen, Takashi Yokota, Md Mahdi Hasan-Olive, Niloofar Sherazi, Nima Borhan Fakouri, Claus Desler, Christine Elisabeth Regnell, Steen Larsen, Lene Juel Rasmussen, Flemming Dela, Linda Hildegard Bergersen, Martin Lauritzen
Brain aging is accompanied by declining mitochondrial respiration. We hypothesized that mitochondrial morphology and dynamics would reflect this decline. Using hippocampus and frontal cortex of a segmental progeroid mouse model lacking Cockayne syndrome protein B (CSB(m/m)) and C57Bl/6 (WT) controls and comparing young (2-5 months) to middle-aged mice (13-14 months), we found that complex I-linked state 3 respiration (CI) was reduced at middle age in CSB(m/m) hippocampus, but not in CSB(m/m) cortex or WT brain...
August 12, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29031722/activated-macrophages-control-human-adipocyte-mitochondrial-bioenergetics-via-secreted-factors
#13
Michaela Keuper, Stephan Sachs, Ellen Walheim, Lucia Berti, Bernhard Raedle, Daniel Tews, Pamela Fischer-Posovszky, Martin Wabitsch, Martin Hrabě de Angelis, Gabi Kastenmüller, Matthias H Tschöp, Martin Jastroch, Harald Staiger, Susanna M Hofmann
OBJECTIVE: Obesity-associated WAT inflammation is characterized by the accumulation and local activation of macrophages (MΦs), and recent data from mouse studies suggest that macrophages are modifiers of adipocyte energy metabolism and mitochondrial function. As mitochondrial dysfunction has been associated with obesity and the metabolic syndrome in humans, herein we aimed to delineate how human macrophages may affect energy metabolism of white adipocytes. METHODS: Human adipose tissue gene expression analysis for markers of macrophage activation and tissue inflammation (CD11c, CD40, CD163, CD206, CD80, MCP1, TNFα) in relationship to mitochondrial complex I (NDUFB8) and complex III (UQCRC2) was performed on subcutaneous WAT of 24 women (BMI 20-61 kg/m(2))...
October 2017: Molecular Metabolism
https://www.readbyqxmd.com/read/29031197/mitochondrial-dysfunction-is-responsible-for-fatty-acid-synthase-inhibition-induced-apoptosis-in-breast-cancer-cells-by-pdpamn
#14
Qiang Wang, Xia Du, Bingjie Zhou, Jing Li, Wenlong Lu, Qiuyun Chen, Jing Gao
Targeting cellular metabolism is becoming a hallmark to overcome drug resistance in breast cancer treatment. Activation of fatty acid synthase (FASN) has been shown to promote breast cancer cell growth. However, there is no concrete report underlying the mechanism associated with mitochondrial dysfunction in relation to fatty acid synthase inhibition-induced apoptosis in breast cancer cells. The current study is aimed at exploring the effect of the novel manganese (Mn) complex, labeled as PdpaMn, on lipid metabolism and mitochondrial function in breast cancer cells...
October 11, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29031071/discovery-of-thienopyrrolotriazine-derivatives-to-protect-mitochondrial-function-against-a%C3%AE-induced-neurotoxicity
#15
TaeHun Kim, Woo Seung Son, Mohammad Neaz Morshed, Ashwini M Londhe, Seo Yun Jung, Jong-Hyun Park, Woo-Kyu Park, Sang Min Lim, Ki Duk Park, Sung Jin Cho, Kyu-Sung Jeong, Jiyoun Lee, Ae Nim Pae
Recovery of mitochondrial dysfunction has gained increasing attention as an alternative therapeutic strategy for Alzheimer's disease (AD). Recent studies suggested that the 18 kDa mitochondrial translocator protein (TSPO) has the potential to serve as a drug target for the treatment of AD. In this study, we generated a structure-based pharmacophore model and virtually screened a commercial library, identifying SVH07 as a virtual hit, which contained a tricyclic core structure, thieno[2',3':4,5]pyrrolo[1,2-d][1,2,4]triazine group...
September 21, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29031050/paraquat-affects-mitochondrial-bioenergetics-dopamine-system-expression-and-locomotor-activity-in-zebrafish-danio-rerio
#16
Xiao H Wang, Christopher L Souders, Yuan H Zhao, Christopher J Martyniuk
The dipyridyl herbicide paraquat induces oxidative stress in cells and is implicated in adult neurodegenerative diseases. However, less is known about paraquat toxicity in early stages of vertebrate development. To address this gap, zebrafish (Danio rerio) embryos were exposed to 1, 10 and 100 μM paraquat for 96 h. Paraquat did not induce significant mortality nor deformity in embryos and larvae, but it did accelerate time to hatch. To evaluate whether mitochondrial respiration was related to earlier hatch times, oxygen consumption rate was measured in whole embryos...
October 6, 2017: Chemosphere
https://www.readbyqxmd.com/read/29030986/the-small-molecule-au14022-promotes-colorectal-cancer-cell-death-via-p53-mediated-g2-m-phase-arrest-and-mitochondria-mediated-apoptosis
#17
Hwani Ryu, Ky-Youb Nam, Jae Sung Kim, Sang-Gu Hwang, Jie-Young Song, Jiyeon Ahn
The p53 tumor suppressor plays critical roles in cell cycle regulation and apoptotic cell death, with its activation capable of sensitizing cancer cells to radiotherapy or chemotherapy. To identify small molecules that induce apoptosis via increased p53 transcriptional activity, we used a novel in-house library containing 96 small-molecule compounds. Using a cell-based screening method with a p53-responsive luciferase-reporter assay system involving benzoxazole derivatives, we found that AU14022 administration significantly increased p53 transcriptional activity in a concentration-dependent manner...
October 14, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29030588/impaired-branched-chain-amino-acid-metabolism-may-underlie-the-nonalcoholic-fatty-liver-disease-like-pathology-of-neonatal-testosterone-treated-female-rats
#18
Álvaro Anzai, Rodrigo R Marcondes, Thiago H Gonçalves, Kátia C Carvalho, Manuel J Simões, Natália Garcia, José M Soares, Vasantha Padmanabhan, Edmund C Baracat, Ismael D C G da Silva, Gustavo A R Maciel
Polycystic ovary syndrome (PCOS) is frequently associated with non-alcoholic fatty liver disease (NAFLD), but the mechanisms involved in the development of NAFLD in PCOS are not well known. We investigated histological changes and metabolomic profile in the liver of rat models of PCOS phenotype induced by testosterone or estradiol. Two-day old female rats received sc injections of 1.25 mg testosterone propionate (Testos; n = 10), 0.5 mg estradiol benzoate (E2; n = 10), or vehicle (control group, CNT; n = 10)...
October 13, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29030260/cyanidin-3-o-glucoside-promotes-the-biosynthesis-of-progesterone-through-the-protection-of-mitochondrial-function-in-pb-exposed-rat-leydig-cells
#19
Luona Wen, Xinwei Jiang, Jianxia Sun, Xia Li, Xusheng Li, Lingmin Tian, Ye Li, Weibin Bai
Cyanidin-3-O-glucoside (C3G) is an anthocyanin that has been reported to reduce the toxicity of heavy metals. In the present study, the protection effects of C3G on the biosynthesis of progesterone, the precursor of testosterone, against lead (Pb) in R2C rat Leydig cells were examined. Treatment of R2C cells with 100 μM Pb resulted in a significant decrease in progesterone production. After being cultured in a medium containing C3G and Pb, R2C cells exhibited an increase in progesterone concentration compared with the Pb treatment, as a result of up-regulation of the expression of the steroidogenic enzymes steroidogenic acute regulatory protein (StAR), 3β-hydroxysteroid dehydrogenase (3β-HSD) and cytochrome P450 enzyme cholesterol side chain cleavage enzyme (CYP11A1)...
October 10, 2017: Food and Chemical Toxicology
https://www.readbyqxmd.com/read/29030231/als-associated-mutation-sod1-g93a-leads-to-abnormal-mitochondrial-dynamics-in-osteocytes
#20
Huan Wang, Jianxun Yi, Xuejun Li, Yajuan Xiao, Kamal Dhakal, Jingsong Zhou
While the death of motor neuron is a pathological hallmark of amyotrophic lateral sclerosis (ALS), defects in other cell types or organs may also actively contribute to ALS disease progression. ALS patients experience progressive skeletal muscle wasting that may not only exacerbate neuronal degeneration, but likely has a significant impact on bone function. In our previous published study, we have discovered severe bone loss in an ALS mouse model with overexpression of ALS-associated mutation SOD1(G93A) (G93A)...
October 10, 2017: Bone
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