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Mitophagy

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https://www.readbyqxmd.com/read/28935571/aggravated-post-infarct-heart-failure-in-type-2-diabetes-is-associated-with-impaired-mitophagy-and-exaggerated-inflammasome-activation
#1
Thota Durga Devi, Mohan Babu, Petri Mäkinen, Minna Kaikkonen, Merja Heinaniemi, Hanne Laakso, Elias Ylä-Herttuala, Lassi Rieppo, Timo Liimatainen, Nikolay Naumenko, Pasi Tavi, Seppo Ylä-Herttuala
Type 2 diabetes mellitus (T2DM) is a major risk factor for heart disease. Mortality rates following myocardial infarction (MI) are significantly increased in T2DM patients due to dysfunctional left ventricle (LV). However, molecular pathways underlying accelerated post-MI heart failure (HF) in T2DM remain unclear. We investigated the underlying mechanisms by inducing MI in a well-established model of T2DM and control mice. Cardiac imaging revealed a significantly decreased global LV ejection fraction (EF) in parallel with increased mortality post-MI in T2DM mice compared to controls...
September 18, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28930681/parkin-independent-mitophagy-controls-chemotherapeutic-response-in-cancer-cells
#2
Elodie Villa, Emma Proïcs, Camila Rubio-Patiño, Sandrine Obba, Barbara Zunino, Jozef P Bossowski, Romain M Rozier, Johanna Chiche, Laura Mondragón, Joel S Riley, Sandrine Marchetti, Els Verhoeyen, Stephen W G Tait, Jean-Ehrland Ricci
Mitophagy is an evolutionarily conserved process that selectively targets impaired mitochondria for degradation. Defects in mitophagy are often associated with diverse pathologies, including cancer. Because the main known regulators of mitophagy are frequently inactivated in cancer cells, the mechanisms that regulate mitophagy in cancer cells are not fully understood. Here, we identified an E3 ubiquitin ligase (ARIH1/HHARI) that triggers mitophagy in cancer cells in a PINK1-dependent manner. We found that ARIH1/HHARI polyubiquitinates damaged mitochondria, leading to their removal via autophagy...
September 19, 2017: Cell Reports
https://www.readbyqxmd.com/read/28925688/live-cell-imaging-of-mitochondrial-autophagy-with-a-novel-fluorescent-small-molecule
#3
Hidefumi Iwashita, Satoru Torii, Noriyoshi Nagahora, Munetaka Ishiyama, Kosei Shioji, Kazumi Sasamoto, Shigeomi Shimizu, Kentaro Okuma
There has been a growing interest in mitophagy, mitochondria-selective autophagy, which plays an essential role in maintaining intracellular homeostasis. We have developed a small-molecule fluorescent probe, Mtphagy Dye, for visualizing mitophagy, which was readily synthesized from a known perylene derivative, perylene-3,4-dicarboxylic anhydride. Mtphagy Dye has suitable fluorescent properties for detecting mitochondrial acidification during mitophagy in the long-wavelength region that does not damage mitochondria...
September 21, 2017: ACS Chemical Biology
https://www.readbyqxmd.com/read/28917714/mitochondria-in-the-nervous-system-from-health-to-disease-part-i
#4
EDITORIAL
Brian M Polster, Maria Teresa Carrì, Philip M Beart
In Part I of this Special Issue on "Mitochondria in the Nervous System: From Health to Disease", the editors bring together contributions from experts in brain mitochondrial research to provide an up-to-date overview of mitochondrial functioning in physiology and pathology. The issue provides cutting edge reviews on classical areas of mitochondrial biology that include energy substrate utilization, calcium handling, mitochondria-endoplasmic reticulum communication, and cell death regulation. Additional reviews and original research articles touch upon key mitochondrial defects seen across multiple neurodegenerative conditions, including fragmentation, loss of respiratory capacity, calcium overload, elevated reactive oxygen species generation, perturbed NAD(+) metabolism, altered protein acetylation, and compromised mitophagy...
September 13, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28916822/ampk-phosphorylation-of-ulk1-is-required-for-targeting-of-mitochondria-to-lysosomes-in-exercise-induced-mitophagy
#5
Rhianna C Laker, Joshua C Drake, Rebecca J Wilson, Vitor A Lira, Bevan M Lewellen, Karen A Ryall, Carleigh C Fisher, Mei Zhang, Jeffrey J Saucerman, Laurie J Goodyear, Mondira Kundu, Zhen Yan
Mitochondrial health is critical for skeletal muscle function and is improved by exercise training through both mitochondrial biogenesis and removal of damaged/dysfunctional mitochondria via mitophagy. The mechanisms underlying exercise-induced mitophagy have not been fully elucidated. Here, we show that acute treadmill running in mice causes mitochondrial oxidative stress at 3-12 h and mitophagy at 6 h post-exercise in skeletal muscle. These changes were monitored using a novel fluorescent reporter gene, pMitoTimer, that allows assessment of mitochondrial oxidative stress and mitophagy in vivo, and were preceded by increased phosphorylation of AMP activated protein kinase (Ampk) at tyrosine 172 and of unc-51 like autophagy activating kinase 1 (Ulk1) at serine 555...
September 15, 2017: Nature Communications
https://www.readbyqxmd.com/read/28915410/aiegens-for-biological-process-monitoring-and-disease-theranostics
#6
REVIEW
Xinggui Gu, Ryan T K Kwok, Jacky W Y Lam, Ben Zhong Tang
Biological processes are of great significance for the normal physiological functions of living organisms and closely related to the health. Monitoring of biological processes and diagnosis of diseases based on fluorescent techniques would provide comprehensive insight into mechanism of life and pathogenesis of diseases, precisely guiding therapeutic effect in theranostics. It largely relied on fluorophores with the properties of excellent photostability, large Stokes shift, high signal-to-noise ratio and free of aggregation-caused quenching (ACQ) effect...
November 2017: Biomaterials
https://www.readbyqxmd.com/read/28915329/mitophagy-as-a-protective-mechanism-against-myocardial-stress
#7
Jihoon Nah, Shigeki Miyamoto, Junichi Sadoshima
Mitochondria are dynamic organelles that can undergo fusion, fission, biogenesis, and autophagic elimination to maintain mitochondrial quality control. Since the heart is in constant need of high amounts of energy, mitochondria, as a central energy supply source, play a crucial role in maintaining optimal cardiac performance. Therefore, it is reasonable to assume that mitochondrial dysfunction is associated with the pathophysiology of heart diseases. In non-dividing, post-mitotic cells such as cardiomyocytes, elimination of dysfunctional organelles is essential to maintaining cellular function because non-dividing cells cannot dilute dysfunctional organelles through cell division...
September 12, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28914970/microrna-410-is-involved-in-mitophagy-after-cardiac-ischemia-reperfusion-injury-by-targeting-high-mobility-group-box-1-protein
#8
Fan Yang, Tong Li, Zhihuan Dong, Rui Mi
Mitochondrial dysfunction has emerged as a critical pathophysiological factor of myocardial ischemia/reperfusion (I/R) injury. A thorough understanding of mitochondrial dysfunction during I/R at the molecular level is urgently needed. One prominent microRNA, miR-410, was previously reported to be dynamically regulated in diverse cardiomyopathies, but its mechanism is unclear. In the present study, in a cardiac I/R injury mice model, the expression of miR-410 was significantly upregulated, accompanied with decreased mitochondrial function and mitophagy deficit...
September 15, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28914586/presenilins-at-the-crossroad-of-a-functional-interplay-between-park2-parkin-and-pink1-to-control-mitophagy-implication-for-neurodegenerative-diseases
#9
Frédéric Checler, Thomas Goiran, Cristine Alves da Costa
Autophagic and mitophagic defects are consistently observed in Alzheimer's disease-affected brains. However, the mechanistic defects underlying these anatomical lesions remained unexplained. We have delineated a molecular cascade by which PSEN1 and PSEN2 (presenilins 1 and 2) control PINK1 transcription and function by an AICD-mediated FOXO3a-dependent mechanism. Further, we establish that PARK2 (parkin) acts upstream to PINK1 and regulates its function by a PSEN-dependent mechanism. Our study thus demonstrates a functional interplay between PSEN and PINK1 and establishes a feedback process by which PARK2 and PINK1 could control mitochondrial dysfunction and autophagic processes in various neurodegenerative pathologies including Alzheimer's and Parkinson's diseases...
September 15, 2017: Autophagy
https://www.readbyqxmd.com/read/28906548/activation-of-g-protein-coupled-estrogen-receptor-1-at-the-onset-of-reperfusion-protects-the-myocardium-against-ischemia-reperfusion-injury-by-reducing-mitochondrial-dysfunction-and-mitophagy
#10
Yansheng Feng, Ngonidzashe B Madungwe, Carolina Victoria da Cruz Junho, Jean C Bopassa
BACKGROUND AND PURPOSE: Recent evidence indicates that Gper1 (G Protein-coupled Estrogen Receptor 1) mediates acute pre-ischemic estrogen-induced protection of the myocardium from ischemia/reperfusion injury via a signaling cascade that includes PKC translocation, ERK1/2 /GSK-3β phosphorylation and the inhibition of the mitochondrial permeability transition pore (mPTP) opening. Here, we investigated the impact and mechanism involved in post-ischemic Gper1 activation in ischemia/reperfusion injury...
September 14, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28900532/mitochondrial-function-and-mitophagy-in-the-elderly-effects-of-exercise
#11
REVIEW
Osvaldo C Moreira, Brisamar Estébanez, Susana Martínez-Florez, José A de Paz, María J Cuevas, Javier González-Gallego
Aging is a natural, multifactorial and multiorganic phenomenon wherein there are gradual physiological and pathological changes over time. Aging has been associated with a decrease of autophagy capacity and mitochondrial functions, such as biogenesis, dynamics, and mitophagy. These processes are essential for the maintenance of mitochondrial structural integrity and, therefore, for cell life, since mitochondrial dysfunction leads to an impairment of energy metabolism and increased production of reactive oxygen species, which consequently trigger mechanisms of cellular senescence and apoptotic cell death...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28895489/effects-of-mild-running-on-substantia-nigra-during-early-neurodegeneration
#12
Michael F Almeida, Carolliny M Silva, Rodrigo S Chaves, Nathan C R Lima, Renato S Almeida, Karla P Melo, Marilene Demasi, Tiago Fernandes, Edilamar M Oliveira, Luis E S Netto, Sandra M Cardoso, Merari F R Ferrari
Moderate physical exercise acts at molecular and behavioural levels, such as interfering in neuroplasticity, cell death, neurogenesis, cognition and motor functions. Therefore, the aim of this study is to analyse the cellular effects of moderate treadmill running upon substantia nigra during early neurodegeneration. Aged male Lewis rats (9-month-old) were exposed to rotenone 1mg/kg/day (8 weeks) and 6 weeks of moderate treadmill running, beginning 4 weeks after rotenone exposure. Substantia nigra was extracted and submitted to proteasome and antioxidant enzymes activities, hydrogen peroxide levels and Western blot to evaluate tyrosine hydroxylase (TH), alpha-synuclein, Tom-20, PINK1, TrkB, SLP1, CRMP-2, Rab-27b, LC3II and Beclin-1 level...
September 12, 2017: Journal of Sports Sciences
https://www.readbyqxmd.com/read/28894028/mtorc1-regulates-both-general-autophagy-and-mitophagy-induction-after-oxidative-phosphorylation-uncoupling
#13
Alberto Bartolomé, Ana García-Aguilar, Shun-Ichiro Asahara, Yoshiaki Kido, Carlos Guillén, Utpal B Pajvani, Manuel Benito
The mechanistic target of rapamycin complex 1 (MTORC1) is a critical negative regulator of general autophagy. We hypothesized that MTORC1 may specifically regulate autophagic clearance of damaged mitochondria. To test this, we used cells lacking tuberous sclerosis complex 2 (TSC2 -/-), which show constitutive MTORC1 activation. TSC2 -/- cells show MTORC1-dependent impaired autophagic flux after chemical uncoupling of mitochondria, increased mitochondrial protein aging and accumulation of p62/SQSTM1 positive mitochondria...
September 11, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28893839/mitochondrial-fission-facilitates-the-selective-mitophagy-of-protein-aggregates
#14
Jonathon L Burman, Sarah Pickles, Chunxin Wang, Shiori Sekine, Jose Norberto S Vargas, Zhe Zhang, Alice M Youle, Catherine L Nezich, Xufeng Wu, John A Hammer, Richard J Youle
Within the mitochondrial matrix, protein aggregation activates the mitochondrial unfolded protein response and PINK1-Parkin-mediated mitophagy to mitigate proteotoxicity. We explore how autophagy eliminates protein aggregates from within mitochondria and the role of mitochondrial fission in mitophagy. We show that PINK1 recruits Parkin onto mitochondrial subdomains after actinonin-induced mitochondrial proteotoxicity and that PINK1 recruits Parkin proximal to focal misfolded aggregates of the mitochondrial-localized mutant ornithine transcarbamylase (ΔOTC)...
September 11, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28890682/impaired-mitophagy-plays-a-role-in-denervation-of-neuromuscular-junctions-in-als-mice
#15
Robert S Rogers, Sudheer Tungtur, Tomohiro Tanaka, Lisa L Nadeau, Yomna Badawi, Hua Wang, Hong-Min Ni, Wen-Xing Ding, Hiroshi Nishimune
Motor neurons in amyotrophic lateral sclerosis (ALS) patients and animal models show degeneration from the nerve terminal, known as dying-back neuropathy. To investigate the mechanism underlying this neuropathy, we analyzed the neuromuscular junctions (NMJs) and motor neuron cell bodies in SOD1(G93A) mice using electron microscopy. NMJs of SOD1(G93A) mice exhibited significantly higher numbers of autophagosomes and degenerated mitochondria compared to wild-type controls. Mitophagosomes were identified in the NMJ presynaptic terminals of wild-type mice and SOD1(G93A) mice...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28878259/promoting-drp1-mediated-mitochondrial-fission-in-midlife-prolongs-healthy-lifespan-of-drosophila-melanogaster
#16
Anil Rana, Matheus P Oliveira, Andy V Khamoui, Ricardo Aparicio, Michael Rera, Harry B Rossiter, David W Walker
The accumulation of dysfunctional mitochondria has been implicated in aging, but a deeper understanding of mitochondrial dynamics and mitophagy during aging is missing. Here, we show that upregulating Drp1-a Dynamin-related protein that promotes mitochondrial fission-in midlife, prolongs Drosophila lifespan and healthspan. We find that short-term induction of Drp1, in midlife, is sufficient to improve organismal health and prolong lifespan, and observe a midlife shift toward a more elongated mitochondrial morphology, which is linked to the accumulation of dysfunctional mitochondria in aged flight muscle...
September 6, 2017: Nature Communications
https://www.readbyqxmd.com/read/28871145/reversible-keap1-inhibitors-are-preferential-pharmacological-tools-to-modulate-cellular-mitophagy
#17
Nikolaos D Georgakopoulos, Michele Frison, Maria Soledad Alvarez, Hélène Bertrand, Geoff Wells, Michelangelo Campanella
Mitophagy orchestrates the autophagic degradation of dysfunctional mitochondria preventing their pathological accumulation and contributing to cellular homeostasis. We previously identified a novel chemical tool (hereafter referred to as PMI), which drives mitochondria into autophagy without collapsing their membrane potential (ΔΨm). PMI is an inhibitor of the protein-protein interaction (PPI) between the transcription factor Nrf2 and its negative regulator, Keap1 and is able to up-regulate the expression of autophagy-associated proteins, including p62/SQSTM1...
September 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28869833/yap-promotes-hepatocellular-carcinoma-metastasis-and-mobilization-via-governing-cofilin-f-actin-lamellipodium-axis-by-regulation-of-jnk-bnip3-serca-camkii-pathways
#18
Chen Shi, Yong Cai, Yongheng Li, Ye Li, Nan Hu, Sai Ma, Shunying Hu, Pingjun Zhu, Weihu Wang, Hao Zhou
Despite the increasingly important role of Hippo-Yap in hepatocellular carcinoma (HCC) development and progression, little insight is available at the time regarding the specifics interaction of Yap and cancer cells migration. Here, we identified the mechanism by which tumor-intrinsic Yap deletion resulted in HCC migratory inhibition. Yap was greatly upregulated in HCC and its expression promoted the cells migration. Functional studies found that knockdown of Yap induced JNK phosphorylation which closely bound to the Bnip3 promoter and contributed to Bnip3 expression...
August 24, 2017: Redox Biology
https://www.readbyqxmd.com/read/28862956/sirtuin-3-deficiency-accelerates-hypertensive-cardiac-remodeling-by-impairing-angiogenesis
#19
Tong Wei, Gaojian Huang, Jing Gao, Chenglin Huang, Mengwei Sun, Jian Wu, Juan Bu, Weili Shen
BACKGROUND: Emerging evidence indicates that impaired angiogenesis may contribute to hypertension-induced cardiac remodeling. The nicotinamide adenine dinucleotide-dependent deacetylase Sirtuin 3 (SIRT3) has the potential to modulate angiogenesis, but this has not been confirmed. As such, the aim of this study was to examine the relationship between SIRT3-mediated angiogenesis and cardiac remodeling. METHODS AND RESULTS: Our experiments were performed on SIRT3 knockout and age-matched wild-type mice infused with angiotensin II (1400 ng/kg per minute) or saline for 14 days...
August 19, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28859306/il-10-reprogramming-of-metabolism-in-macrophages-through-mitophagy
#20
Jyoti Patel
No abstract text is available yet for this article.
September 1, 2017: Cardiovascular Research
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