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https://www.readbyqxmd.com/read/28526246/impaired-mitophagy-facilitates-mitochondrial-damage-in-danon-disease
#1
Sherin I Hashem, Anne N Murphy, Ajit S Divakaruni, Matthew L Klos, Bradley C Nelson, Emily C Gault, Teisha J Rowland, Cynthia N Perry, Yusu Gu, Nancy D Dalton, William H Bradford, Eric J Devaney, Kirk L Peterson, Kenneth L Jones, Matthew R G Taylor, Ju Chen, Neil C Chi, Eric D Adler
RATIONALE: Lysosomal associated membrane protein type-2 (LAMP-2) is a highly conserved, ubiquitous protein that is critical for autophagic flux. Loss of function mutations in the LAMP-2 gene cause Danon disease, a rare X-linked disorder characterized by developmental delay, skeletal muscle weakness, and severe cardiomyopathy. We previously found that human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from Danon patients exhibited significant mitochondrial oxidative stress and apoptosis...
May 16, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28524859/mesenchymal-stem-cells-sense-mitochondria-released-from-damaged-cells-as-danger-signals-to-activate-their-rescue-properties
#2
Meriem Mahrouf-Yorgov, Lionel Augeul, Claire Crola Da Silva, Maud Jourdan, Muriel Rigolet, Sylvie Manin, René Ferrera, Michel Ovize, Adeline Henry, Aurélie Guguin, Jean-Paul Meningaud, Jean-Luc Dubois-Randé, Roberto Motterlini, Roberta Foresti, Anne-Marie Rodriguez
Mesenchymal stem cells (MSCs) protect tissues against cell death induced by ischemia/reperfusion insults. This therapeutic effect seems to be controlled by physiological cues released by the local microenvironment following injury. Recent lines of evidence indicate that MSC can communicate with their microenvironment through bidirectional exchanges of mitochondria. In particular, in vitro and in vivo studies report that MSCs rescue injured cells through delivery of their own mitochondria. However, the role of mitochondria conveyed from somatic cells to MSC remains unknown...
May 19, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28522765/exercise-training-in-tg%C3%AE-q-44-mice-during-the-progression-of-chronic-heart-failure-cardiac-vs-peripheral-soleus-muscle-impairments-to-oxidative-metabolism
#3
Bruno Grassi, Joanna Majerczak, Eleonora Bardi, Alessia Buso, Marina Comelli, Stefan Chlopicki, Magdalena Guzik, Irene Mavelli, Zenon Nieckarz, Desy Salvadego, Urszula Tyrankiewicz, Tomasz Skorka, Roberto Bottinelli, Jerzy A Zoladz, Maria Antonietta Pellegrino
Cardiac function, skeletal (soleus) muscle oxidative metabolism and the effects of exercise training were evaluated in a transgenic murine model (Tgαq*44) of chronic heart failure (CHF) during the critical period between the occurrence of an impairment of cardiac function and the stage at which overt cardiac failure ensues (i.e. from 10 to 12 months of age). Forty-eight Tgαq*44 mice and 43 wild-type (WT) FVB controls were randomly assigned to control groups and to groups undergoing 2 months of intense exercise training (spontaneous running on a instrumented wheel)...
May 18, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28518143/calcium-sensing-receptor-protects-high-glucose-induced-energy-metabolism-disorder-via-blocking-gp78-ubiquitin-proteasome-pathway
#4
Yuehong Wang, Ping Gao, Can Wei, Hongzhu Li, Li Zhang, Yajun Zhao, Bo Wu, Ye Tian, Weihua Zhang, Lingyun Wu, Rui Wang, Changqing Xu
Diabetic cardiomyopathy (DCM) is a major complication and fatal cause of the patients with diabetes. The calcium sensing receptor (CaSR) is a G protein-coupled receptor, which is involved in maintaining calcium homeostasis, regulating cell proliferation and apoptosis, and so on. In our previous study, we found that CaSR expression, intracellular calcium levels and cardiac function were all significantly decreased in DCM rats; however, the exact mechanism are not clear yet. The present study revealed the protective role of CaSR in myocardial energy metabolism disorder induced by high glucose (HG) as well as the underlying mechanism...
May 18, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28500761/melatonin-ameliorates-myocardial-ischemia-reperfusion-injury-through-sirt3-dependent-regulation-of-oxidative-stress-and-apoptosis
#5
Mengen Zhai, Buying Li, Weixun Duan, Lin Jing, Bin Zhang, Meng Zhang, Liming Yu, Zhenhua Liu, Bo Yu, Kai Ren, Erhe Gao, Yang Yang, Hongliang Liang, Zhenxiao Jin, Shiqiang Yu
Sirtuins are a family of highly evolutionarily conserved nicotinamide adenine nucleotide-dependent histone deacetylases. Sirtuin-3 (SIRT3) is a member of the sirtuin family that is localized primarily to the mitochondria and protects against oxidative stress-related diseases, including myocardial ischemia/reperfusion (MI/R) injury. Melatonin has a favorable effect in ameliorating MI/R injury. We hypothesized that melatonin protects against MI/R injury by activating the SIRT3 signaling pathway. In this study, mice were pre-treated with or without a selective SIRT3 inhibitor and then subjected to MI/R operation...
May 13, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28498888/cardiomyocyte-specific-loss-of-mitochondrial-p32-c1qbp-causes-cardiomyopathy-and-activates-stress-responses
#6
Toshiro Saito, Takeshi Uchiumi, Mikako Yagi, Rie Amamoto, Daiki Setoyama, Yuichi Matsushima, Dongchon Kang
Aims: Mitochondria are important organelles, dedicated to energy production. Mitochondrial p32/C1qbp, which functions as an RNA and protein chaperone, interacts with mitochondrial mRNA and is indispensable for mitochondrial function through its regulation of mitochondrial translation in cultured cell lines. However, the precise role of p32/C1qbp in vivo is poorly understood because of embryonic lethality in the systemic p32-deficient mouse. The goal of this study was to examine the physiological function of mitochondrial p32/C1qbp in the heart...
May 11, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28498411/mitochondrial-activity-and-oxidative-stress-functions-are-influenced-by-the-activation-of-ahr-induced-cyp1a1-overexpression-in-cardiomyocytes
#7
Bing Zhou, Xi Wang, Feng Li, Yingting Wang, Lei Yang, Xiaolong Zhen, Wuhong Tan
There is an endemic cardiomyopathy currently occurring in China, termed, Keshan disease (KD). The authors previously compared mitochondrial‑associated gene expression profiles of peripheral blood mononuclear cells (PBMCs) derived from KD patients and normal controls, using mitochondria‑focused cDNA microarray technology. The results detected an upregulation of the enzyme‑associated CYP1A1 gene, (ratios ≥2.0). The aryl hydrocarbon receptor (AhR) regulates the expression of numerous cytochrome P450 (CYP) genes including members of the CYP1 family; CYP1A1 and CYP1A2...
May 12, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28497127/evidence-of-glycolysis-up-regulation-and-pyruvate-mitochondrial-oxidation-mismatch-during-mechanical-unloading-of-the-failing-human-heart-implications-for-cardiac-reloading-and-conditioning
#8
Nikolaos A Diakos, Sutip Navankasattusas, E Dale Abel, Jared Rutter, Lauren McCreath, Peter Ferrin, Stephen H McKellar, Dylan V Miller, Song Y Park, Russell S Richardson, Ralph Deberardinis, James E Cox, Abdallah G Kfoury, Craig H Selzman, Josef Stehlik, James C Fang, Dean Y Li, Stavros G Drakos
This study sought to investigate the effects of mechanical unloading on myocardial energetics and the metabolic perturbation of heart failure (HF) in an effort to identify potential new therapeutic targets that could enhance the unloading-induced cardiac recovery. The authors prospectively examined paired human myocardial tissue procured from 31 advanced HF patients at left ventricular assist device (LVAD) implant and at heart transplant plus tissue from 11 normal donors. They identified increased post-LVAD glycolytic metabolites without a coordinate increase in early, tricarboxylic acid (TCA) cycle intermediates...
October 2016: JACC. Basic to Translational Science
https://www.readbyqxmd.com/read/28493473/dysregulation-of-mitochondrial-bioenergetics-and-quality-control-by-hiv-1-tat-in-cardiomyocytes
#9
Farzaneh G Tahrir, Santhanam Shanmughapriya, Taha Mohseni Ahooyi, Tijana Knezevic, Manish K Gupta, Christopher D Kontos, Joseph M McClung, Muniswamy Madesh, Jennifer Gordon, Arthur M Feldman, Joseph Y Cheung, Kamel Khalili
Cardiovascular disease remains a leading cause of morbidity and mortality in HIV positive patients, even in those whose viral loads are well controlled with antiretroviral therapy. However, the underlying molecular events responsible for the development of cardiac disease in the setting of HIV remain unknown. The HIV encoded Tat protein plays a critical role in the activation of HIV gene expression and profoundly impacts homeostasis in both HIV infected cells and uninfected cells that have taken up released Tat via a bystander effect...
May 11, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28493471/what-role-does-the-stress-response-have-in-congestive-heart-failure
#10
REVIEW
Ahmed Badreddin, Youssef Fady, Hamdy Attia, Mohamed Hafez, Ahmed Khairallah, Dina Johar, Larry Bernstein
This review is concerned with cardiac malfunction as a result of an imbalance in protein proteostasis, the homeostatic balance between protein removal and regeneration in a long remodeling process involving the endoplasmic reticulum (ER) and the unfolded protein response (UPR). The importance of this is of special significance with regard to cardiac function as a high energy requiring muscular organ that has a high oxygen requirement and is highly dependent on mitochondria. The importance of mitochondria is not only concerned with high energy dependence on mitochondrial electron transport, but it also has a role in the signaling between the mitochondria and the ER under stress...
May 11, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28478705/rejuvenation-of-cardiac-tissue-developed-from-reprogrammed-aged-somatic-cells
#11
Zhao Cheng, Hong-Ling Peng, Rong Zhang, Xian-Ming Fu, Guang-Sen Zhang
Induced pluripotent stem cells (iPSCs) derived through somatic cell reprogramming have been reported to reset aged somatic cells to a more youthful state, characterized by elongated telomeres, a rearranged mitochondrial network, reduced oxidative stress and restored pluripotency. However, it is still unclear whether the reprogrammed aged somatic cells can function normally as embryonic stem cells (ESCs) during development and be rejuvenated. In the current study, we applied the aggregation technique to investigate whether iPSCs derived from aged somatic cells could develop normally and be rejuvenated...
May 6, 2017: Rejuvenation Research
https://www.readbyqxmd.com/read/28463107/pde2a2-regulates-mitochondria-morphology-and-apoptotic-cell-death-via-local-modulation-of-camp-pka-signalling
#12
Stefania Monterisi, Miguel J Lobo, Craig Livie, John C Castle, Michael Weinberger, George Baillie, Nicoletta C Surdo, Nshunge Musheshe, Alessandra Stangherlin, Eyal Gottlieb, Rory Maizels, Mario Bortolozzi, Massimo Micaroni, Manuela Zaccolo
cAMP/PKA signalling is compartmentalised with tight spatial and temporal control of signal propagation underpinning specificity of response. The cAMP-degrading enzymes, phosphodiesterases (PDEs), localise to specific subcellular domains within which they control local cAMP levels and are key regulators of signal compartmentalisation. Several components of the cAMP/PKA cascade are located to different mitochondrial sub-compartments, suggesting the presence of multiple cAMP/PKA signalling domains within the organelle...
May 2, 2017: ELife
https://www.readbyqxmd.com/read/28457864/development-or-disease-duality-of-the-mitochondrial-permeability-transition-pore
#13
REVIEW
María José Pérez, Rodrigo A Quintanilla
Mitochondria is not only a dynamic organelle that produces ATP, but is also an important contributor to cell functions in both development and cell death processes. These paradoxical functions of mitochondria are partially regulated by the mitochondrial permeability transition pore (mPTP), a high-conductance channel that can induce loss of mitochondrial membrane potential, impairment of cellular calcium homeostasis, oxidative stress, and a decrease in ATP production upon pathological activation. Interestingly, despite their different etiologies, several neurodegenerative diseases and heart ischemic injuries share mitochondrial dysfunction as a common element...
April 28, 2017: Developmental Biology
https://www.readbyqxmd.com/read/28450119/role-of-the-calcium-sensing-receptor-in-cardiomyocyte-apoptosis-via-mitochondrial-dynamics-in-compensatory-hypertrophied-myocardium-of-spontaneously-hypertensive-rat
#14
Siting Hong, Xin Zhang, Xiaohui Zhang, Wenxiu Liu, Yu Fu, Yue Liu, Zhiyu Shi, Jinyu Chi, Meng Zhao, Xinhua Yin
Calcium sensing receptor (CaSR) mediates pathological cardiac hypertrophy. Mitochondria maintain their function through fission and fusion and disruption of mitochondrial dynamic is linked to various cardiac diseases. This study examined how inhibition of CaSR by the inhibitor Calhex231 affected the mitochondrial dynamics in a hypertensive model in rats. Spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were used in this study. Cardiac function and blood pressure was evaluated at the end of the study...
April 24, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28449155/mitochondrial-dysfunction-in-diabetic-cardiomyopathy-effect-of-mesenchymal-stem-cell-with-ppar-%C3%AE-agonist-or-exendin-4
#15
Mohamed Abd Elaziz Wassef, Ola M Tork, Laila A Rashed, Walaa Ibrahim, Heba Morsi, Dina Mohamed Mekawy Rabie
Therapy targeting mitochondria may provide novel ways to treat diabetes and its complications. Bone marrow-derived mesenchymal stem cells (MSCs), the peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists and exendin-4; an analog of glucagon-like peptide-1 have shown cardioprotective properties in many cardiac injury models. So, we evaluated their effects in diabetic cardiomyopathy (DCM) in relation to mitochondrial dysfunction. This work included seven groups of adult male albino rats: the control group, the non-treated diabetic group, and the treated diabetic groups: one group was treated with MSCs only, the second with pioglitazone only, the third with MSCs and pioglitazone, the forth with exendin-4 only and the fifth with MSCs and exendin-4...
April 27, 2017: Experimental and Clinical Endocrinology & Diabetes
https://www.readbyqxmd.com/read/28439028/bgp-15-prevents-the-death-of-neurons-in-a-mouse-model-of-familial-dysautonomia
#16
Sarah B Ohlen, Magdalena L Russell, Michael J Brownstein, Frances Lefcort
Hereditary sensory and autonomic neuropathy type III, or familial dysautonomia [FD; Online Mendelian Inheritance in Man (OMIM) 223900], affects the development and long-term viability of neurons in the peripheral nervous system (PNS) and retina. FD is caused by a point mutation in the gene IKBKAP/ELP1 that results in a tissue-specific reduction of the IKAP/ELP1 protein, a subunit of the Elongator complex. Hallmarks of the disease include vasomotor and cardiovascular instability and diminished pain and temperature sensation caused by reductions in sensory and autonomic neurons...
April 24, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28433661/differential-protein-acetylation-assists-import-of-excess-sod2-into-mitochondria-and-mediates-sod2-aggregation-associated-with-cardiac-hypertrophy-in-the-murine-sod2-tg-heart
#17
Liwen Zhang, Chwen-Lih Chen, Patrick T Kang, Zhicheng Jin, Yeong-Renn Chen
SOD2 is the primary antioxidant enzyme neutralizing (•)O2(-) in mitochondria. Cardiac-specific SOD2 overexpression (SOD2-tg) induces supernormal function and cardiac hypertrophy in the mouse heart. However, the reductive stress imposed by SOD2 overexpression results in protein aggregation of SOD2 pentamers and differential hyperacetylation of SOD2 in the mitochondria and cytosol. Here, we studied SOD2 acetylation in SOD2-tg and wild-type mouse hearts. LC-MS/MS analysis indicated the presence of four acetylated lysines in matrix SOD2 and nine acetylated lysines in cytosolic SOD2 from the SOD2-tg heart...
April 20, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28432072/translocase-of-inner-membrane-50-functions-as-a-novel-protective-regulator-of-pathological-cardiac-hypertrophy
#18
Kai Tang, Yifan Zhao, Hailing Li, Mengyun Zhu, Weiming Li, Weijing Liu, Guofu Zhu, Dachun Xu, Wenhui Peng, Ya-Wei Xu
BACKGROUND: Translocase of inner membrane 50 (TIM50) is a member of the translocase of inner membrane (TIM) complex in the mitochondria. Previous research has demonstrated the role of TIM50 in the regulation of oxidative stress and cardiac morphology. However, the role of TIM50 in pathological cardiac hypertrophy remains unknown. METHODS AND RESULTS: In the present study we found that the expression of TIM50 was downregulated in hypertrophic hearts. Using genetic loss-of-function animal models, we demonstrated that TIM50 deficiency increased heart and cardiomyocyte size with more severe cardiac fibrosis compared with wild-type littermates...
April 21, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28423723/honokiol-an-activator-of-sirtuin-3-sirt3-preserves-mitochondria-and-protects-the-heart-from-doxorubicin-induced-cardiomyopathy-in-mice
#19
Vinodkumar B Pillai, Abhinav Kanwal, Yong Hu Fang, Willard W Sharp, Sadhana Samant, Jack Arbiser, Mahesh P Gupta
Doxorubicin is the chemotherapeutic drug of choice for a wide variety of cancers, and cardiotoxicity is one of the major side effects of doxorubicin treatment. One of the main cellular targets of doxorubicin in the heart is mitochondria. Mitochondrial sirtuin, SIRT3 has been shown to protect against doxorubicin-induced cardiotoxicity. We have recently identified honokiol (HKL) as an activator of SIRT3, which protects the heart from developing pressure overload hypertrophy. Here, we show that HKL-mediated activation of SIRT3 also protects the heart from doxorubicin-induced cardiac damage without compromising the tumor killing potential of doxorubicin...
March 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28423313/power-grid-protection-of-the-muscle-mitochondrial-reticulum
#20
Brian Glancy, Lisa M Hartnell, Christian A Combs, Armel Fenmou, Junhui Sun, Elizabeth Murphy, Sriram Subramaniam, Robert S Balaban
Mitochondrial network connectivity enables rapid communication and distribution of potential energy throughout the cell. However, this connectivity puts the energy conversion system at risk, because damaged elements could jeopardize the entire network. Here, we demonstrate the mechanisms for mitochondrial network protection in heart and skeletal muscle (SKM). We find that the cardiac mitochondrial reticulum is segmented into subnetworks comprising many mitochondria linked through abundant contact sites at highly specific intermitochondrial junctions (IMJs)...
April 18, 2017: Cell Reports
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