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Cardiac autophagy

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https://www.readbyqxmd.com/read/29223072/alteration-of-autophagy-related-proteins-in-peripheral-blood-mononuclear-cells-of-patients-with-parkinson-s-disease
#1
Yasuo Miki, Shuji Shimoyama, Tomoya Kon, Tatsuya Ueno, Ryo Hayakari, Kunikazu Tanji, Tomoh Matsumiya, Eiki Tsushima, Fumiaki Mori, Koichi Wakabayashi, Masahiko Tomiyama
Previous postmortem studies demonstrated dysregulation of autophagy in patients with Parkinson's disease (PD). To clarify whether this alteration reflects a fundamental aspect of PD or represents the final stage of autophagy dysregulation resulting from a long neurodegenerative process, we focused on basal autophagy in peripheral blood mononuclear cells (PBMCs) of PD patients (n = 35) and controls (n = 23). The whole-transcriptome assay revealed downregulation of mRNAs for 6 core regulators of autophagy (UNC-51-like kinase [ULK] 3, autophagy-related [Atg] 2A, Atg4B, Atg5, Atg16L1, and histone deacetylase 6)...
November 21, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/29216769/zinc-prevents-mitochondrial-superoxide-generation-by-inducing-mitophagy-in-the-setting-of-hypoxia-reoxygenation-in-cardiac-cells
#2
Xiyun Bian, Tianming Teng, Huanhuan Zhao, Jiangyu Qin, Zhen Qiao, Yuemin Sun, Zhiqiang Liun, Zhelong Xu
Zinc plays a role in autophagy and protects cardiac cells from ischemia/reperfusion injury. This study aimed to test if zinc can induce mitophagy leading to attenuation of mitochondrial superoxide generation in the setting of hypoxia/reoxygenation (H/R) in cardiac cells. H9c2 cells were subjected to 4 h hypoxia followed by 2 h reoxygenation. Under normoxic conditions, treatments of cells with ZnCl2 increased both the LC3-II/LC3-I ratio and GFP-LC3 puncta, implying that zinc induces autophagy. Further experiments showed that endogenous zinc is required for the autophagy induced by starvation and rapamycin...
December 7, 2017: Free Radical Research
https://www.readbyqxmd.com/read/29215735/vacuolated-pas-positive-lymphocytes-as-an-hallmark-of-pompe-disease-and-other-myopathies-related-to-impaired-autophagy
#3
Angelo Pascarella, Chiara Terracciano, Olimpia Farina, Luca Lombardi, Teresa Esposito, Filomena Napolitano, Giuseppina Franzese, Giovanni Panella, Francesco Tuccillo, Giancarlo la Marca, Sergio Bernardini, Silvia Boffo, Antonio Giordano, Mariarosa Anna Beatrice Melone, Giuseppe Di Iorio, Simone Sampaolo
Autosomal recessive Pompe disease is a lysosomal disorder caused by mutations of the acid-α-glucosidase (GAA) gene. Deficiency of GAA enzyme leads to glycogen accumulation and autophagy impairment in cardiac and skeletal muscles, but also in lymphocytes. Since an effective therapy is available, a rapid, sensitive and specific test is crucial to early identify affected subjects. Number of lymphocytes containing PAS-positive vacuoles was evaluated on blood films from 72 consecutive adult patients with hyperckemia and/or muscle weakness, 13 genetically confirmed late-onset-Pompe-disease (LOPD) and 13 of their offspring...
December 7, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29212794/ferroptosis-beating-on-death-s-door
#4
Rimpy Dhingra, Amir Ravandi, Lorrie A Kirshenbaum
One of the most fascinating concepts to impact contemporary biology to date is the idea that cell death is a highly regulated and programmed event. Cardiac cells can die by apoptosis or necrosis and in some instances by autophagy. Ferroptosis, is a new form of regulated cell death that is gaining considerable attention, that links de-regulated iron metabolism with peroxidative lipid injury. In this report, we highlight a recent study by Baba et al that describes ferroptosis as regulated form of cell death in the heart...
December 6, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/29207125/the-spectrum-of-myocardial-homeostasis-mechanisms-in-the-settings-of-cardiac-surgery-procedures-review
#5
Emmanuel Papadakis, Meletios Kanakis, Agapi Kataki, Demetrios A Spandidos
Classic cardiac surgery, determined through the function of cardiopulmonary bypass machine and myocardial cardioplegic arrest, represents the most controlled scenario for cardiomyocyte homeostatic disturbances due to systemic inflammatory response and myocardial reperfusion injury. An increasing number of studies have demonstrated that myocardial cell homeostasis in cardiac surgery procedures is a sequence of molecularly interrelated and overlapping mechanisms in the form of apoptosis, autophagy and necrosis, which are activated by a plethora of induced inflammatory mediators and gene‑related signaling pathways...
November 28, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29206300/effects-of-mtor-nf-%C3%AE%C2%BAb-signaling-pathway-and-high-thoracic-epidural-anesthesia-on-myocardial-ischemia-reperfusion-injury-via-autophagy-in-rats
#6
Wei-Qiang Huang, Jian-Lin Wen, Ri-Qi Lin, Peng Wei, Feng Huang
We investigated the role of mammalian target of rapamycin/nuclear factor-kappa B (mTOR/NF-κB) signaling pathway in high thoracic epidural anesthesia (HTEA) against myocardial ischemia-reperfusion (I/R) injury in rats. The rat model of myocardial I/R injury was established. Ninety rats were divided into the normal, sham, I/R, eHTEA, the PDTC and HTEA + PDTC groups. ELISA was applied to detect cardiac function indexes. HE staining was conducted to observe histopathological changes of myocardial tissues, and TTC staining was performed to detect the myocardial infarction size...
December 5, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/29203581/cardiac-insulin-signaling-regulates-glycolysis-through-phosphofructokinase-2-content-and-activity
#7
Lee B Bockus, Satoshi Matsuzaki, Shraddha S Vadvalkar, Zachary T Young, Jennifer R Giorgione, Maria F Newhardt, Michael Kinter, Kenneth M Humphries
BACKGROUND: The healthy heart has a dynamic capacity to respond and adapt to changes in nutrient availability. Diabetes mellitus disrupts this metabolic flexibility and promotes cardiomyopathy through mechanisms that are not completely understood. Phosphofructokinase 2 (PFK-2) is a primary regulator of cardiac glycolysis and substrate selection, yet its regulation under normal and pathological conditions is unknown. This study was undertaken to determine how changes in insulin signaling affect PFK-2 content, activity, and cardiac metabolism...
December 4, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29203562/impaired-protein-quality-control-during-left-ventricular-remodeling-in-mice-with-cardiac-restricted-overexpression-of-tumor-necrosis-factor
#8
Justin Hartupee, Gabor D Szalai, Wei Wang, Xiucui Ma, Abhinav Diwan, Douglas L Mann
BACKGROUND: Sustained inflammation in the heart is sufficient to provoke left ventricular dysfunction and left ventricular remodeling. Although inflammation has been linked to many of the biological changes responsible for adverse left ventricular remodeling, the relationship between inflammation and protein quality control in the heart is not well understood. METHODS AND RESULTS: To study the relationship between chronic inflammation and protein quality control, we used a mouse model of dilated cardiomyopathy driven by cardiac restricted overexpression of TNF (tumor necrosis factor; Myh6-sTNF)...
December 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/29187515/nrf2-at-the-heart-of-oxidative-stress-and-cardiac-protection
#9
Qin M Chen, Anthony J Maltagliati
The NFE2L2 gene encodes the transcription factor Nrf2 best known for regulating the expression of antioxidant and detoxification genes. Gene knockout approaches have demonstrated its universal cytoprotective features. While Nrf2 has been the topic of intensive research in cancer biology since its discovery in 1994, understanding the role of Nrf2 in cardiovascular disease has just begun. The literature concerning Nrf2 in experimental models of atherosclerosis, ischemia, reperfusion, cardiac hypertrophy, heart failure, and diabetes supports its cardiac protective character...
November 29, 2017: Physiological Genomics
https://www.readbyqxmd.com/read/29184499/aliskiren-improves-ischemia-and-oxygen-glucose-deprivation-induced-cardiac-injury-through-activation-of-autophagy-and-amp-activated-protein-kinase
#10
Ming-Hsien Chiang, Chan-Jung Liang, Chen-Wei Liu, Bo-Jhih Pan, Wen-Ping Chen, Yi-Fan Yang, I-Ta Lee, Jaw-Shiun Tsai, Chiang-Wen Lee, Yuh-Lien Chen
Aliskiren is a direct renin inhibitor that has been effective in anti-hypertension. We investigated whether aliskiren could improve the ischemia-induced cardiac injury and whether the autophagy was involved in this effect. A myocardial infarction (MI) model was created by the ligation of the left anterior coronary artery in C57J/BL6 mice. They were treated for 1, 3, 7, and 14 days with vehicle or aliskiren (25 mg/kg/day via subcutaneous injection). In vivo, the MI mice exhibited worse cardiac function by echocardiographic assessment and showed larger myocardial scarring by light microscopy, whereas aliskiren treatment reversed these effects, which were also associated with the changes in caspase-3 and Bcl-2 expression as well as in the number of apoptotic cells...
2017: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29174818/inhibition-of-advanced-glycation-endproduct-age-rescues-against-streptozotocin-induced-diabetic-cardiomyopathy-role-of-autophagy-and-er-stress
#11
Zhaohui Pei, Qinqin Deng, Sara A Babcock, Emily Y He, Jun Ren, Yingmei Zhang
Diabetes mellitus leads to oxidative stress and contractile dysfunction in the heart. Although several rationales have been speculated, the precise mechanism behind diabetic cardiomyopathy remains elusive. This study was designed to assess the role of inhibition of advanced glycation endproducts (AGE) in streptozotocin (STZ)-induced diabetic cardiac dysfunction. Cardiac contractile function was assessed in normal C57BL/6 and STZ (200mg/kg, single injection and maintained for 2 wks)-induced diabetic mice treated with or without the AGE inhibitor aminoguanidine (50mg/kg/d in drinking water) for 2 weeks using echocardiography and IonOptix MyoCam techniques...
November 22, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/29161706/endotoxin-effects-on-cardiac-and-renal-functions-and-cardiorenal-syndromes
#12
Grazia Maria Virzì, Anna Clementi, Alessandra Brocca, Claudio Ronco
Gram-negative sepsis is a major cause of morbidity and mortality in critical ill patients. Recent findings in molecular biology and in signaling pathways have enhanced our understanding of its pathogenesis and opened up opportunities of innovative therapeutic approaches. Endotoxin plays a pivotal role in the pathogenesis of multi-organ dysfunction in the setting of gram-negative sepsis. Indeed, heart and kidney impairments seem to be induced by the release of circulating pro-inflammatory and pro-apoptotic mediators triggered by endotoxin interaction with immune cells...
November 22, 2017: Blood Purification
https://www.readbyqxmd.com/read/29157081/regulation-of-becn1-mediated-autophagy-by-hspb6-insights-from-a-human-hspb6-s10f-mutant
#13
Guan-Sheng Liu, Hongyan Zhu, Wen-Feng Cai, Xiaohong Wang, Min Jiang, Kobina Essandoh, Elizabeth Vafiadaki, Kobra Haghighi, Chi Keung Lam, George Gardner, George Adly, Persoulla Nicolaou, Despina Sanoudou, Qiangrong Liang, Jack Rubinstein, Guo-Chang Fan, Evangelia G Kranias
HSPB6/Hsp20 (heat shock protein family B [small] member 6) has emerged as a novel cardioprotector against stress-induced injury. We identified a human mutant of HSPB6 (HSPB6(S10F)) exclusively present in dilated cardiomyopathy (DCM) patients. Cardiac expression of this mutant in mouse hearts resulted in remodeling and dysfunction, which progressed to heart failure and early death. These detrimental effects were associated with reduced interaction of mutant HSPB6(S10F) with BECN1/Beclin 1, leading to BECN1 ubiquitination and its proteosomal degradation...
November 20, 2017: Autophagy
https://www.readbyqxmd.com/read/29149759/dusp1-alleviates-cardiac-ischemia-reperfusion-injury-by-suppressing-the-mff-required-mitochondrial-fission-and-bnip3-related-mitophagy-via-the-jnk-pathways
#14
Qinhua Jin, Ruibing Li, Nan Hu, Ting Xin, Pingjun Zhu, Shunying Hu, Sai Ma, Hong Zhu, Jun Ren, Hao Zhou
Mitochondrial fission and selective mitochondrial autophagy (mitophagy) form an essential axis of mitochondrial quality control that plays a critical role in the development of cardiac ischemia-reperfusion (IR) injury. However, the precise upstream molecular mechanism of fission/mitophagy remains unclear. Dual-specificity protein phosphatase1 (DUSP1) regulates cardiac metabolism, but its physiological contribution in the reperfused heart, particularly its influence on mitochondrial homeostasis, is unknown. Here, we demonstrated that cardiac DUSP1 was downregulated following acute cardiac IR injury...
November 6, 2017: Redox Biology
https://www.readbyqxmd.com/read/29143784/primary-cilium-dependent-signaling-mechanisms
#15
REVIEW
Rajasekharreddy Pala, Nedaa Alomari, Surya M Nauli
Primary cilia are hair-like organelles and play crucial roles in vertebrate development, organogenesis, health, and many genetic disorders. A primary cilium is a mechano-sensory organelle that responds to mechanical stimuli in the micro-environment. A cilium is also a chemosensor that senses chemical signals surrounding a cell. The overall function of a cilium is therefore to act as a communication hub to transfer extracellular signals into intracellular responses. Although intracellular calcium has been one of the most studied signaling messengers that transmit extracellular signals into the cells, calcium signaling by various ion channels remains a topic of interest in the field...
October 28, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29141547/cardioprotective-effects-of-serca2a-overexpression-against-ischemia-reperfusion-induced-injuries-in-rats
#16
Yan Jian, Li-Li Tian, Lin-Hui Wang, Xiao-Dong Zhao, Jing-Wei Chen, Koji Murao, Wei Zhu, Liang Dong, Guo-Qing Wang, Wan-Ping Sun, Guo-Xing Zhang
AIMS: The aim of the present study is to assess how genetically increased Sarcoplasmic reticulum Ca2+-ATPase (Serca2a) expression affects cardiac injury after ischemia/reperfusion (I/R) exposure and the related mechanisms involved. METHODS AND RESULTS: Rats were subjected to left anterior descending coronary artery (LAD) occlusion for 30 min followed by a 24-hour reperfusion. Cardiac function analysis revealed that cardiac function dramatically improved in Serca2a transgenic rats (Serca2aTG) rats compared to wild type (WT) rats...
November 10, 2017: Current Gene Therapy
https://www.readbyqxmd.com/read/29137484/the-role-of-endogenous-reactive-oxygen-species-in-cardiac-myocyte-autophagy
#17
J-P Wang, R-F Chi, J Liu, Y-Z Deng, X-B Han, F-Z Qin, B Li
Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations. However, little is known about the influences of physiological levels of endogenous ROS on cardiomyocyte autophagy. In the present study, we tested the hypothesis that endogenous ROS in cardiomyocytes play an important role in inducing autophagy. Cultured H9C2 cardiomyocytes or Sprague-Dawley rats were treated with the antioxidant N-acetyl-cysteine (NAC) or the superoxide dismutase mimic tempol under the basal or nutrient deprivation conditions...
November 10, 2017: Physiological Research
https://www.readbyqxmd.com/read/29134574/correction-to-potential-signaling-pathways-of-acute-endurance-exercise-induced-cardiac-autophagy-and-mitophagy-and-its-possible-role-in-cardioprotection
#18
Youngil Lee, Insu Kwon, Yongchul Jang, Wankeun Song, Ludmila M Cosio-Lima, Mark H Roltsch
The article Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection, written by Youngil Lee.
November 13, 2017: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/29129702/fkbp8-protects-the-heart-from-hemodynamic-stress-by-preventing-the-accumulation-of-misfolded-proteins-and-endoplasmic-reticulum-associated-apoptosis-in-mice
#19
Tomofumi Misaka, Tomokazu Murakawa, Kazuhiko Nishida, Yosuke Omori, Manabu Taneike, Shigemiki Omiya, Chris Molenaar, Yoshihiro Uno, Osamu Yamaguchi, Junji Takeda, Ajay M Shah, Kinya Otsu
Protein quality control in cardiomyocytes is crucial to maintain cellular homeostasis. The accumulation of damaged organelles, such as mitochondria and misfolded proteins in the heart is associated with heart failure. During the process to identify novel mitochondria-specific autophagy (mitophagy) receptors, we found FK506-binding protein 8 (FKBP8), also known as FKBP38, shares similar structural characteristics with a yeast mitophagy receptor, autophagy-related 32 protein. However, knockdown of FKBP8 had no effect on mitophagy in HEK293 cells or H9c2 myocytes...
November 10, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29127187/apobec2-deficiency-causes-mitochondrial-defects-and-mitophagy-in-skeletal-muscle
#20
Yusuke Sato, Hideaki Ohtsubo, Naohiro Nihei, Takane Kaneko, Yoriko Sato, Shin-Ichi Adachi, Shinji Kondo, Mako Nakamura, Wataru Mizunoya, Hiroshi Iida, Ryuichi Tatsumi, Cristina Rada, Fumiaki Yoshizawa
Apobec2 is a member of the activation-induced deaminase/apolipoprotein B mRNA editing enzyme catalytic polypeptide cytidine deaminase family expressed in differentiated skeletal and cardiac muscle. We previously reported that Apobec2 deficiency in mice leads to a shift in muscle fiber type, myopathy, and diminished muscle mass. However, the mechanisms of myopathy caused by Apobec2 deficiency and its physiologic functions are unclear. Here we show that, although Apobec2 localizes to the sarcomeric Z-lines in mouse tissue and cultured myotubes, the sarcomeric structure is not affected in Apobec2-deficient muscle...
November 10, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
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