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mitochondrial autophagy

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https://www.readbyqxmd.com/read/28334504/redd1-deficiency-impairs-autophagy-and-mitochondrial-biogenesis-in-articular-cartilage-and-increases-the-severity-of-experimental-osteoarthritis
#1
Oscar Alvarez-Garcia, Tokio Matsuzaki, Merissa Olmer, Lars Plate, Jeffery W Kelly, Martin K Lotz
Objective REDD1 is an endogenous inhibitor of mTOR that regulates cellular stress responses. REDD1 expression is decreased in aged and osteoarthritis (OA) cartilage and it regulates mTOR signaling and autophagy in articular chondrocytes in vitro. The present study investigated the effects of REDD1 deletion in vivo using a mouse model of experimental OA. Methods Severity of OA was histologically assessed in 4-month-old wild-type and in Redd1(-/-) mice subjected to surgical destabilization of the medial meniscus (DMM)...
March 23, 2017: Arthritis & Rheumatology
https://www.readbyqxmd.com/read/28331313/involvement-of-pink1-parkin-mediated-mitophagy-in-zno-nanoparticle-induced-toxicity-in-bv-2-cells
#2
Limin Wei, Jianfeng Wang, Aijie Chen, Jia Liu, Xiaoli Feng, Longquan Shao
With the increasing application of zinc oxide nanoparticles (ZnO NPs) in biological materials, the neurotoxicity caused by these particles has raised serious concerns. However, the underlying molecular mechanisms of the toxic effect of ZnO NPs on brain cells remain unclear. Mitochondrial damage has been reported to be a factor in the toxicity of ZnO NPs. PINK1/parkin-mediated mitophagy is a newly emerging additional function of autophagy that selectively degrades impaired mitochondria. Here, a PINK1 gene knockdown BV-2 cell model was established to determine whether PINK1/parkin-mediated mitophagy was involved in ZnO NP-induced toxicity in BV-2 cells...
2017: International Journal of Nanomedicine
https://www.readbyqxmd.com/read/28330601/mitochondria-in-cell-senescence-is-mitophagy-the-weakest-link
#3
REVIEW
Viktor I Korolchuk, Satomi Miwa, Bernadette Carroll, Thomas von Zglinicki
Cell senescence is increasingly recognized as a major contributor to the loss of health and fitness associated with aging. Senescent cells accumulate dysfunctional mitochondria; oxidative phosphorylation efficiency is decreased and reactive oxygen species production is increased. In this review we will discuss how the turnover of mitochondria (a term referred to as mitophagy) is perturbed in senescence contributing to mitochondrial accumulation and Senescence-Associated Mitochondrial Dysfunction (SAMD). We will further explore the subsequent cellular consequences; in particular SAMD appears to be necessary for at least part of the specific Senescence-Associated Secretory Phenotype (SASP) and may be responsible for tissue-level metabolic dysfunction that is associated with aging and obesity...
March 14, 2017: EBioMedicine
https://www.readbyqxmd.com/read/28329063/lysosomal-proteolysis-is-associated-with-exercise-induced-improvement-of-mitochondrial-quality-control-in-aged-hippocampus
#4
Li Luo, Jia-Ru Dai, Shan-Shan Guo, A-Ming Lu, Xiao-Fang Gao, Yan-Rong Gu, Xiao-Fei Zhang, Hai-Dong Xu, Yan Wang, Zhou Zhu, Lisa J Wood, Zheng-Hong Qin
Exercise improves cognitive function in older adults, but the underlying mechanism is largely unknown. Both lysosomal degradation and mitochondrial quality control decline with age. We hypothesized that exercise ameliorates age-related cognitive decline through the improvement of mitochondrial quality control in aged hippocampus, and this effect is associated with lysosomal proteolysis. Sixteen to eighteen-month old male Sprague Dawley rats underwent swim exercise training for 10 weeks. The exercise regimen prevented cognitive decline in aged rats, reduced oxidative stress, and rejuvenated mitochondria in the aged hippocampus...
January 19, 2017: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
https://www.readbyqxmd.com/read/28324658/mitochondrial-respiration-links-tor-complex-2-signaling-to-calcium-regulation-and-autophagy
#5
Ariadne Vlahakis, Nerea Lopez Muniozguren, Ted Powers
The Target of Rapamycin (TOR) kinase is a conserved regulator of cell growth and functions within 2 different protein complexes, TORC1 and TORC2, where TORC2 positively controls macroautophagy/autophagy during amino acid starvation. Under these conditions, TORC2 signaling inhibits the activity of the calcium-regulated phosphatase calcineurin and promotes the general amino acid control (GAAC) response and autophagy. Here we demonstrate that TORC2 regulates calcineurin by controlling the respiratory activity of mitochondria...
March 21, 2017: Autophagy
https://www.readbyqxmd.com/read/28324492/detection-of-hypoxia-induced-and-iron-depletion-induced-mitophagy-in-mammalian-cells
#6
Shun-Ichi Yamashita, Tomotake Kanki
Mitochondrial quality and quantity are not only regulated by mitochondrial fusion and fission but also by mitochondria degradation. Mitophagy, an autophagy specific for damaged or unnecessary mitochondria, is believed to be an important pathway for mitochondrial homeostasis. To date, several stimuli are known to induce mitophagy. Some of these stimuli, however, including hypoxia, iron depletion, and nitrogen starvation, induce mild mitophagy, which is difficult to detect through decreased mitochondrial mass...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324487/mitophagy-in-yeast-a-screen-of-mitophagy-deficient-mutants
#7
Kentaro Furukawa, Tomotake Kanki
Mitochondrial autophagy (mitophagy) is a process that selectively degrades mitochondria via autophagy. Recent studies have shown that mitophagy plays an important role in mitochondrial homeostasis by degrading damaged or excess mitochondria. The budding yeast Saccharomyces cerevisiae is a powerful model organism that has been employed to study several biological phenomena. Recently, there has been significant progress in the understanding of mitophagy in yeast following the identification of Atg32, a mitochondrial outer membrane receptor protein for mitophagy...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324201/potential-roles-of-mitochondria-associated-er-membranes-mams-in-traumatic-brain-injury
#8
REVIEW
Dongdong Sun, Xin Chen, Gang Gu, Jianhao Wang, Jianning Zhang
The endoplasmic reticulum (ER) and mitochondria have both been shown to be critical in cellular homeostasis. The functions of the ER and mitochondria are independent but interrelated. These two organelles could form physical interactions, known as MAMs, to regulate physiological functions between ER and mitochondria to maintain Ca(2+), lipid, and metabolite exchange. Several proteins are located in MAMs, including RNA-dependent protein kinase (PKR)-like ER kinase, inositol 1,4,5-trisphosphate receptors, phosphofurin acidic cluster sorting protein-2 and sigma-1 receptor to ensure regulation...
March 21, 2017: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/28323020/metabolic-reprogramming-in-cancer-cells-consequences-on-ph-and-tumour-progression-integrated-therapeutic-perspectives-with-dietary-lipids-as-adjuvant-to-anticancer-treatment
#9
REVIEW
Jean-François Dumas, Lucie Brisson, Stéphan Chevalier, Karine Mahéo, Gaëlle Fromont, Driffa Moussata, Pierre Besson, Sébastien Roger
While tumours arise from acquired mutations in oncogenes or tumour-suppressor genes, it is clearly established that cancers are metabolic diseases characterized by metabolic alterations in tumour cells, and also non-tumour cells of the host organism resulting in tumour cachexia and patient weakness. In this review, we aimed at delineating details by which metabolic alterations in cancer cells, characterized by mitochondrial bioenergetics deregulations and the preference for aerobic glycolysis, are critical parameters controlling the aggressive progression of tumours...
March 17, 2017: Seminars in Cancer Biology
https://www.readbyqxmd.com/read/28322544/graphene-oxide-quantum-dots-as-novel-nanozymes-for-alcohol-intoxication
#10
Anqi Sun, Li Mu, Xiangang Hu
Alcohol overconsumption as a worldwide issue results in alcoholic liver disease (ALD), such as steatosis, alcoholic hepatitis and cirrhosis. The treatment of ALD has been widely investigated but remains challenging. In this work, the protective effects of graphene oxide quantum dots (GOQDs) as novel nanozymes against alcohol overconsumption are discovered, and the specific mechanisms underlying these effects are elucidated via omics analysis. GOQDs dramatically alleviate the reduction of cell viability induced by ethanol and can act as nanozymes to accelerate ethanol metabolism and avoid the accumulation of toxic intermediates in cells...
March 21, 2017: ACS Applied Materials & Interfaces
https://www.readbyqxmd.com/read/28320515/hmgcs2-promotes-autophagic-degradation-of-the-amyloid-%C3%AE-precursor-protein-through-ketone-body-mediated-mechanisms
#11
Li-Tian Hu, Bing-Lin Zhu, Yu-Jie Lai, Yan Long, Jing-Si Zha, Xiao-Tong Hu, John H Zhang, Guo-Jun Chen
HMGCS2 (mitochondrial 3-hydroxy-3-methylglutaryl-COA synthase 2) is a control enzyme in ketogenesis. The mitochondrial localization and interaction with APP (β-amyloid precursor protein) suggest that HMGCS2 may play a role in the pathophysiology of AD (Alzheimer's disease). Here we report that overexpression of HMGCS2 decreased levels of APP and related CTFs (carboxy-terminal fragments), which was largely prevented by an autophagic inhibitor chloroquine. In addition, HMGCS2 enhancement of autophagic marker LC3II was diminished by rapamycin, an inhibitor of mechanistic target of rapamycin...
March 17, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28302704/swimming-attenuates-d-galactose-induced-brain-aging-via-suppressing-mir-34a-mediated-autophagy-impairment-and-abnormal-mitochondrial-dynamics
#12
Xianjuan Kou, Jie Li, Xingran Liu, Jingru Chang, Qingxia Zhao, Shaohui Jia, Jingjing Fan, Ning Chen
MicroRNAs (miRNAs) have been reported to be involved in many neurodegenerative diseases. In order to explore the regulatory role of miR-34a in aging-related diseases such as Alzheimer's disease (AD) during exercise intervention, we constructed a rat model with (D-galactose) D-gal-induced oxidative stress and cognitive impairment coupled with dysfunctional autophagy and abnormal mitochondrial dynamics, determined the mitigation of cognitive impairment of D-gal-induced aging rats during swimming intervention, and evaluated miR-34a-mediated functional status of autophagy and abnormal mitochondrial dynamics...
March 16, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28301876/autophagy-inhibitor-chloroquine-increases-sensitivity-to-cisplatin-in-qbc939-cholangiocarcinoma-cells-by-mitochondrial-ros
#13
Xianzhi Qu, Jiyao Sheng, Luyan Shen, Jing Su, Yunjie Xu, Qi Xie, Yao Wu, Xuewen Zhang, Liankun Sun
The tumor cells have some metabolic characteristics of the original tissues, and the metabolism of the tumor cells is closely related to autophagy. However, the mechanism of autophagy and metabolism in chemotherapeutic drug resistance is still poorly understood. In this study, we investigated the role and mechanism of autophagy and glucose metabolism in chemotherapeutic drug resistance by using cholangiocarcinoma QBC939 cells with primary cisplatin resistance and hepatocellular carcinoma HepG2 cells. We found that QBC939 cells with cisplatin resistance had a higher capacity for glucose uptake, consumption, and lactic acid generation, and higher activity of the pentose phosphate pathway compared with HepG2 cells, and the activity of PPP was further increased after cisplatin treatment in QBC939 cells...
2017: PloS One
https://www.readbyqxmd.com/read/28301072/pre-conditions-for-eliminating-mitochondrial-dysfunction-and-maintaining-liver-function-after-hepatic-ischaemia-reperfusion
#14
REVIEW
Chenxia Hu, Lanjuan Li
The liver, the largest organ with multiple synthesis and secretion functions in mammals, consists of hepatocytes and Kupffer, stem, endothelial, stellate and other parenchymal cells. Because of early and extensive contact with the external environment, hepatic ischaemia reperfusion (IR) may result in mitochondrial dysfunction, autophagy and apoptosis of cells and tissues under various pathological conditions. Because the liver requires a high oxygen supply to maintain normal detoxification and synthesis functions, it is extremely susceptible to ischaemia and subsequent reperfusion with blood...
March 16, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28298952/insights-for-oxidative-stress-and-mtor-signaling-in-myocardial-ischemia-reperfusion-injury-under-diabetes
#15
REVIEW
Dajun Zhao, Jian Yang, Lifang Yang
Diabetes mellitus (DM) displays a high morbidity. The diabetic heart is susceptible to myocardial ischemia/reperfusion (MI/R) injury. Impaired activation of prosurvival pathways, endoplasmic reticulum (ER) stress, increased basal oxidative state, and decreased antioxidant defense and autophagy may render diabetic hearts more vulnerable to MI/R injury. Oxidative stress and mTOR signaling crucially regulate cardiometabolism, affecting MI/R injury under diabetes. Producing reactive oxygen species (ROS) and reactive nitrogen species (RNS), uncoupling nitric oxide synthase (NOS), and disturbing the mitochondrial quality control may be three major mechanisms of oxidative stress...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28297802/-influence-of-high-fat-diet-in-paternal-c57bl-6-mice-on-liver-fat-deposition-in-offspring
#16
J Zhang, H G Li, L Fu, F S Di
Objective: To investigate the influence of high-fat diet (HFD) in paternal C57BL/6 mice on HFD-induced liver fat deposition in male offspring, as well as transgenerational inheritance caused by paternal HFD and related mechanisms. Methods: A total of 20 male C57BL/6 mice aged 3 weeks (F0) were randomly divided into normal control group (C, 10 mice) and HFD group (HF, 10 mice). After 12 weeks of HFD intervention, the male mice in the HFD group mated with female ones treated with normal diet and pups were obtained...
February 20, 2017: Zhonghua Gan Zang Bing za Zhi, Zhonghua Ganzangbing Zazhi, Chinese Journal of Hepatology
https://www.readbyqxmd.com/read/28296000/novel-application-of-localized-nanodelivery-of-anti-il6-protects-organ-transplant-from-ischemia-reperfusion-injuries
#17
Zhabiz Solhjou, Mayuko Uehara, Baharak Bahmani, Omar H Maarouf, Takaharu Ichimura, Craig R Brooks, Wanlong Xu, Mine Yilmaz, Abdala Elkhal, Stefan G Tullius, Indira Guleria, Martina McGrath, Reza Abdi
Ischemia reperfusion injury (IRI) evokes intra-graft inflammatory responses, which markedly augment alloimmune responses against the graft. Understanding the mechanisms underlying these responses is fundamental to develop therapeutic regimens to prevent/ameliorate organ IRI. Here, we demonstrate that IRI results in a marked increase in mitochondrial damage and autophagy in dendritic cells (DC). While autophagy is a survival mechanism for ischemic DC, it also augments their production of IL6. Allograft derived dendritic cells (ADDC) lacking autophagy related gene 5 (Atg5) showed higher death rates post-transplantation...
March 12, 2017: American Journal of Transplantation
https://www.readbyqxmd.com/read/28294175/the-age-associated-loss-of-ischemic-preconditioning-in-the-kidney-is-accompanied-by-mitochondrial-dysfunction-increased-protein-acetylation-and-decreased-autophagy
#18
Stanislovas S Jankauskas, Irina B Pevzner, Nadezda V Andrianova, Ljubava D Zorova, Vasily A Popkov, Denis N Silachev, Nataliya G Kolosova, Egor Y Plotnikov, Dmitry B Zorov
In young rats, ischemic preconditioning (IPC), which consists of 4 cycles of ischemia and reperfusion alleviated kidney injury caused by 40-min ischemia. However,old rats lost their ability to protect the ischemic kidney by IPC. A similar aged phenotype was demonstrated in 6-month-old OXYS rats having signs of premature aging. In the kidney of old and OXYS rats, the levels of acetylated nuclear proteins were higher than in young rats, however, unlike in young rats, acetylation levels in old and OXYS rats were further increased after IPC...
March 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28289521/l-carnitine-protects-c2c12-cells-against-mitochondrial-superoxide-overproduction-and-cell-death
#19
Françoise Le Borgne, Gaétan Ravaut, Arnaud Bernard, Jean Demarquoy
AIM: To identify and characterize the protective effect that L-carnitine exerted against an oxidative stress in C2C12 cells. METHODS: Myoblastic C2C12 cells were treated with menadione, a vitamin K analog that engenders oxidative stress, and the protective effect of L-carnitine (a nutrient involved in fatty acid metabolism and the control of the oxidative process), was assessed by monitoring various parameters related to the oxidative stress, autophagy and cell death...
February 26, 2017: World Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28287478/myocardial-ischemic-postconditioning-promotes-autophagy-against-ischemia-reperfusion-injury-via-the-activation-of-the-nnos-ampk-mtor-pathway
#20
Maojuan Hao, Suhua Zhu, Liang Hu, Hongyi Zhu, Xiaowei Wu, Qingping Li
Autophagy participates in the progression of many diseases, comprising ischemia/ reperfusion (I/R). It is reported that it is involved in the protective mechanism of ischemic postconditioning (IPostC). According to research, neuronal nitric oxide synthase (nNOS) is also involved in the condition of I/R and IPostC. However, the relationship between nNOS, autophagy and IPostC has not been previously investigated. We hypothesize that IPostC promotes autophagy activity against I/R injury partially through nNOS-mediated pathways...
March 11, 2017: International Journal of Molecular Sciences
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