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Mitophagy

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https://www.readbyqxmd.com/read/29330382/sesn2-facilitates-mitophagy-by-helping-parkin-translocation-through-ulk1-mediated-beclin1-phosphorylation
#1
Ashish Kumar, Chandrima Shaha
Mitophagy, the selective degradation of mitochondria by autophagy, is crucial for the maintenance of healthy mitochondrial pool in cells. The critical event in mitophagy is the translocation of cytosolic Parkin, a ubiquitin ligase, to the surface of defective mitochondria. This study elucidates a novel role of SESN2/Sestrin2, a stress inducible protein, in mitochondrial translocation of PARK2/Parkin during mitophagy. The data demonstrates that SESN2 downregulation inhibits BECN1/Beclin1 and Parkin interaction, thereby preventing optimum mitochondrial accumulation of Parkin...
January 12, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29328405/liraglutide-repairs-the-infarcted-heart-the-role-of-the-sirt1-parkin-mitophagy-pathway
#2
Huiying Qiao, Haiyan Ren, He Du, Minfang Zhang, Xiaofang Xiong, Rong Lv
Liraglutide is glucagon‑like peptide‑1 receptor agonist used for treating patients with type 2 diabetes mellitus. The present study aimed to investigate the role and mechanism of liraglutide in repairing the infarcted heart following myocardial infarction. The results of the present study demonstrated that amplification of the dose of liraglutide for ~28 days was able to reduce cardiac fibrosis, inflammatory responses and myocardial death in the post‑infarcted heart. In vitro, liraglutide protected cardiomyocyte mitochondria against the chronic hypoxic damage, inhibiting the mitochondrial apoptosis pathways...
January 2, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29325568/pink1-import-regulation-a-fine-system-to-convey-mitochondrial-stress-to-the-cytosol
#3
REVIEW
Shiori Sekine, Richard J Youle
Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway...
January 10, 2018: BMC Biology
https://www.readbyqxmd.com/read/29321664/mitochondrial-fission-and-mitophagy-depend-on-cofilin-mediated-actin-depolymerization-activity-at-the-mitochondrial-fission-site
#4
Guo-Bing Li, Hong-Wei Zhang, Ruo-Qiu Fu, Xiao-Ye Hu, Lei Liu, Yu-Nong Li, Yan-Xia Liu, Xin Liu, Jin-Jiao Hu, Qin Deng, Qing-Song Luo, Rong Zhang, Ning Gao
Mitochondria fission and mitophagy are fundamentally crucial to cellular physiology and play important roles in cancer progression. Developing a comprehensive understanding of the molecular mechanism underlying mitochondrial fission and mitophagy will provide novel strategies for cancer prevention and treatment. Actin has been shown to participate in mitochondrial fission and mitophagy regulation. Cofilin is best known as an actin-depolymerizing factor. However, the molecular mechanism by which cofilin regulates mitochondrial fission and mitophagy remains largely unknown...
January 11, 2018: Oncogene
https://www.readbyqxmd.com/read/29316798/regulation-of-mitophagy-by-the-ubiquitin-pathway-in-neurodegenerative-diseases
#5
Shyamal Desai, Meredith Juncker, Catherine Kim
Mitophagy is a cellular process by which dysfunctional mitochondria are degraded via autophagy. Increasing empirical evidence proposes that this mitochondrial quality-control mechanism is defective in neurons of patients with various neurodegenerative diseases such as Ataxia Telangiectasia, Alzheimer's disease, Parkinson's disease, and Amyotrophic Lateral Sclerosis. Accumulation of defective mitochondria and the production of reactive oxygen species due to defective mitophagy have been identified as causes underlying neurodegenerative disease pathogenesis...
January 1, 2018: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/29316632/excessive-endoplasmic-reticulum-stress-correlates-with-impaired-mitochondrial-dynamics-mitophagy-and-apoptosis-in-liver-and-adipose-tissue-but-not-in-muscles-in-ems-horses
#6
Krzysztof Marycz, Katarzyna Kornicka, Jolanta Szlapka-Kosarzewska, Christine Weiss
Nowadays, endocrine disorders have become more frequent in both human and veterinary medicine. In horses, reduced physical activity combined with carbohydrate and sugar overload may result in the development of the so-called equine metabolic syndrome (EMS). EMS is characterized by insulin resistance, hyperinsulinemia, elevated blood triglyceride concentrations and usually obesity. Although the phenotypic features of EMS individuals are well known, the molecular mechanism underlying disease development remains elusive...
January 6, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29313453/a-pink1-mediated-mitophagy-pathway-decides-the-fate-of-tumors-to-be-benign-or-malignant
#7
Hui Qian, Xiaojuan Chao, Wen-Xing Ding
Macroautophagy/autophagy plays a dual role in cancer depending on the stage of tumorigenesis. Autophagy prevents tumor initiation by suppressing chronic tissue damage, inflammation, accumulation of damaged organelles and genome instability. Autophagy can also sustain tumor metabolism and provide nutrients for tumor growth and survival via nutrient recycling. Moreover, autophagy is required for benign tumors to progress to malignant tumors. Emerging evidence indicates that autophagy or mitophagy can inactivate tumor suppressors such as TP53/TRP53/p53 to promote tumor progression once carcinogenesis has been initiated...
January 9, 2018: Autophagy
https://www.readbyqxmd.com/read/29313421/mitophagy-and-hepatic-cancer-stem-cells
#8
Jiyoung Lee, Kai Liu, Bangyan Stiles, Jing-Hsiung James Ou
No abstract text is available yet for this article.
January 9, 2018: Autophagy
https://www.readbyqxmd.com/read/29311115/miro-proteins-coordinate-microtubule-and-actin-dependent-mitochondrial-transport-and-distribution
#9
Guillermo López-Doménech, Christian Covill-Cooke, Davor Ivankovic, Els F Halff, David F Sheehan, Rosalind Norkett, Nicol Birsa, Josef T Kittler
In the current model of mitochondrial trafficking, Miro1 and Miro2 Rho-GTPases regulate mitochondrial transport along microtubules by linking mitochondria to kinesin and dynein motors. By generating Miro1/2 double-knockout mouse embryos and single- and double-knockout embryonic fibroblasts, we demonstrate the essential and non-redundant roles of Miro proteins for embryonic development and subcellular mitochondrial distribution. Unexpectedly, the TRAK1 and TRAK2 motor protein adaptors can still localise to the outer mitochondrial membrane to drive anterograde mitochondrial motility in Miro1/2 double-knockout cells...
January 8, 2018: EMBO Journal
https://www.readbyqxmd.com/read/29307555/vps13d-encodes-a-ubiquitin-binding-protein-that-is-required-for-the-regulation-of-mitochondrial-size-and-clearance
#10
Allyson L Anding, Chunxin Wang, Tsun-Kai Chang, Danielle A Sliter, Christine M Powers, Kay Hofmann, Richard J Youle, Eric H Baehrecke
The clearance of mitochondria by autophagy, mitophagy, is important for cell and organism health [1], and known to be regulated by ubiquitin. During Drosophila intestine development, cells undergo a dramatic reduction in cell size and clearance of mitochondria that depends on autophagy, the E1 ubiquitin-activating enzyme Uba1, and ubiquitin [2]. Here we screen a collection of putative ubiquitin-binding domain-encoding genes for cell size reduction and autophagy phenotypes. We identify the endosomal sorting complex required for transport (ESCRT) components TSG101 and Vps36, as well as the novel gene Vps13D...
December 30, 2017: Current Biology: CB
https://www.readbyqxmd.com/read/29307080/inhibition-of-peroxynitrite-induced-mitophagy-activation-attenuates-cerebral-ischemia-reperfusion-injury
#11
Jinghan Feng, Xingmiao Chen, Binghe Guan, Caiming Li, Jinhua Qiu, Jiangang Shen
Activated autophagy/mitophagy has been intensively observed in ischemic brain, but its roles remain controversial. Peroxynitrite (ONOO-), as a representative of reactive nitrogen species, is considered as a critical neurotoxic factor in mediating cerebral ischemia-reperfusion (I/R) injury, but its roles in autophagy/mitophagy activation remain unclear. Herein, we hypothesized that ONOO- could induce PINK1/Parkin-mediated mitophagy activation via triggering dynamin-related protein 1 (Drp1) recruitment to damaged mitochondria, contributing to cerebral I/R injury...
January 6, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29305265/the-nem1-spo7-protein-phosphatase-complex-is-required-for-efficient-mitophagy-in-yeast
#12
Xueyan Xu, Koji Okamoto
Mitochondria-targeted selective autophagy, termed mitophagy, is an evolutionarily conserved process that contributes to mitochondrial quantity and quality control. Mitophagy requires elaborate membrane biogenesis of autophagosomes surrounding mitochondria, although how this process is regulated remains obscure. We show here that mitophagy is strongly suppressed in yeast cells lacking Nem1 or Spo7, two proteins forming a heterodimeric protein phosphatase complex known to be important for proper shaping of the nucleus and endoplasmic reticulum (ER)...
January 2, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29301859/parl-partitions-the-lipid-transfer-protein-stard7-between-the-cytosol-and-mitochondria
#13
Shotaro Saita, Takashi Tatsuta, Philipp A Lampe, Tim König, Yohsuke Ohba, Thomas Langer
Intramembrane-cleaving peptidases of the rhomboid family regulate diverse cellular processes that are critical for development and cell survival. The function of the rhomboid protease PARL in the mitochondrial inner membrane has been linked to mitophagy and apoptosis, but other regulatory functions are likely to exist. Here, we identify the START domain-containing protein STARD7 as an intramitochondrial lipid transfer protein for phosphatidylcholine. We demonstrate that PARL-mediated cleavage during mitochondrial import partitions STARD7 to the cytosol and the mitochondrial intermembrane space...
January 4, 2018: EMBO Journal
https://www.readbyqxmd.com/read/29290944/mitochondrial-targeted-hsp90-inhibitor-gamitrinib-tpp-g-tpp-induces-pink1-parkin-dependent-mitophagy
#14
Fabienne C Fiesel, Elle D James, Roman Hudec, Wolfdieter Springer
Loss-of-function mutations in PINK1 or PARKIN are associated with early-onset Parkinson's disease. Upon mitochondrial stress, PINK1 and Parkin together mediate a response that protects cells from the accumulation of harmful, damaged mitochondria. PINK1, the upstream kinase accumulates on the mitochondrial surface and recruits the E3 ubiquitin ligase Parkin on site to ubiquitylate substrate proteins. The joint activity of both to generate phosphorylated poly-ubiquitin chains on the mitochondrial surface induces the recruitment of autophagy receptors and eventually whole organelles are cleared by autophagy...
December 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/29287956/mitochondrial-quality-control-the-role-of-mitophagy-in-aging
#15
REVIEW
Ruoyang Shi, Matthew Guberman, Lorrie A Kirshenbaum
Autophagy is a catabolic process for eliminating macromolecules and damaged organelles by a highly regulated lysosomal pathway. Importantly, autophagy serves as an integral quality control mechanism by recycling cellular constituents for energy consumption and cellular rejuvenation under basal and stress conditions. Nevertheless, there is growing evidence that under certain conditions autophagy can switch from an adaptive survival mechanism to maladaptive process that promotes cell death. Furthermore, defects in autophagy have been linked to mitochondria injury and cell death associated with aging...
December 6, 2017: Trends in Cardiovascular Medicine
https://www.readbyqxmd.com/read/29286376/in-vitro-and-in-vivo-detection-of-mitophagy-in-human-cells-c-elegans-and-mice
#16
Evandro F Fang, Konstantinos Palikaras, Nuo Sun, Elayne M Fivenson, Ryan D Spangler, Jesse S Kerr, Stephanie A Cordonnier, Yujun Hou, Eszter Dombi, Henok Kassahun, Nektarios Tavernarakis, Joanna Poulton, Hilde Nilsen, Vilhelm A Bohr
Mitochondria are the powerhouses of cells and produce cellular energy in the form of ATP. Mitochondrial dysfunction contributes to biological aging and a wide variety of disorders including metabolic diseases, premature aging syndromes, and neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Maintenance of mitochondrial health depends on mitochondrial biogenesis and the efficient clearance of dysfunctional mitochondria through mitophagy. Experimental methods to accurately detect autophagy/mitophagy, especially in animal models, have been challenging to develop...
November 22, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/29284690/ampk%C3%AE-2-protects-against-the-development-of-heart-failure-by-enhancing-mitophagy-via-pink1-phosphorylation
#17
Bei Wang, Jiali Nie, Lujin Wu, Yangyang Hu, Zeng Wen, Lingli Dong, Ming-Hui Zou, Chen Chen, Dao Wen Wang
Rationale: Mitochondrial dysfunction plays an important role in heart failure (HF). However, the molecular mechanisms regulating mitochondrial functions via selective mitochondrial autophagy (mitophagy) are poorly understood. Objective: We sought to determine the role of AMP-activated protein kinase (AMPK) in selective mitophagy during HF. Methods and Results: An isoform shift from AMPKα2 to AMPKα1 was observed in failing-heart samples from HF patients and transverse aortic constriction (TAC)-induced mice, accompanied by decreased mitophagy and mitochondrial function...
December 28, 2017: Circulation Research
https://www.readbyqxmd.com/read/29277693/current-mechanistic-insights-into-the-cccp-induced-cell-survival-response
#18
REVIEW
Mariame Selma Kane, Aurelien Paris, Philippe Codron, Julien Cassereau, Vincent Procaccio, Guy Lenaers, Pascal Reynier, Arnaud Chevrollier
The ring-substituted derivatives of carbonyl cyanide phenylhydrazone, CCCP and FCCP, are routinely used for the analysis of the mitochondrial function in living cells, tissues, and isolated mitochondrial preparations. CCCP and FCCP are now being increasingly used for investigating the mechanisms of autophagy by inducing mitochondrial degradation through the disruption of the mitochondrial membrane potential (ΔΨm). Sustained perturbation of ΔΨm, which is normally tightly controlled to ensure cell proliferation and survival, triggers various stress pathways as part of the cellular adaptive response, the main components of which are mitophagy and autophagy...
December 22, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29274400/conditional-mitotimer-reporter-mice-for-assessment-of-mitochondrial-structure-oxidative-stress-and-mitophagy
#19
Rebecca J Wilson, Joshua C Drake, Di Cui, Mei Zhang, Heather M Perry, Jennifer A Kashatus, Christine M Kusminski, Philipp E Scherer, David F Kashatus, Mark D Okusa, Zhen Yan
Assessment of structural and functional changes of mitochondria is vital for biomedical research as mitochondria are the power plants essential for biological processes and tissue/organ functions. Others and we have developed a novel reporter gene, pMitoTimer, which codes for a redox sensitive mitochondrial targeted protein that switches from green fluorescence protein (GFP) to red fluorescent protein (DsRed) when oxidized. It has been shown in transfected cells, transgenic C. elegans and Drosophila m., as well as somatically transfected adult skeletal muscle that this reporter gene allows quantifiable assessment of mitochondrial structure, oxidative stress, and lysosomal targeting of mitochondria-containing autophagosomes...
December 20, 2017: Mitochondrion
https://www.readbyqxmd.com/read/29274359/ho-1-mediates-bay-11-7085-induced-ferroptosis
#20
Ling-Chu Chang, Shih-Kai Chiang, Shuen-Ei Chen, Yung-Luen Yu, Ruey-Hwang Chou, Wei-Chao Chang
Ferroptosis is a form of oxidative cell death and has become a chemotherapeutic target for cancer treatment. BAY 11-7085 (BAY), which is a well-known IκBα inhibitor, suppressed viability in cancer cells via induction of ferroptotic death in a NF-κB-independent manner. Reactive oxygen species scavenging, relief of lipid peroxidation, replenishment of glutathione and thiol-containing agents, as well as iron chelation, rescued BAY-induced cell death. BAY upregulated a variety of Nrf2 target genes related to redox regulation, particularly heme oxygenase-1 (HO-1)...
December 20, 2017: Cancer Letters
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