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https://www.readbyqxmd.com/read/28333383/calcium-transport-and-signaling-in-mitochondria
#1
Roberto Bravo-Sagua, Valentina Parra, Camila López-Crisosto, Paula Díaz, Andrew F G Quest, Sergio Lavandero
Calcium (Ca2+) is a key player in the regulation of many cell functions. Just like Ca2+, mitochondria are ubiquitous, versatile, and dynamic players in determining both cell survival and death decisions. Given their ubiquitous nature, the regulation of both is deeply intertwined, whereby Ca2+ regulates mitochondrial functions, while mitochondria shape Ca2+ dynamics. Deregulation of either Ca2+ or mitochondrial signaling leads to abnormal function, cell damage or even cell death, thereby contributing to muscle dysfunction or cardiac pathologies...
March 16, 2017: Comprehensive Physiology
https://www.readbyqxmd.com/read/28333095/cytosolic-bnip3-dimer-interacts-with-mitochondrial-bax-forming-heterodimers-in-the-mitochondrial-outer-membrane-under-basal-conditions
#2
Ulrike B Hendgen-Cotta, Sonja Esfeld, Katharina Rudi, Ilkka Miinalainen, Johann P Klare, Tienush Rassaf
The primary function of mitochondria is energy production, a task of particular importance especially for cells with a high energy demand like cardiomyocytes. The B-cell lymphoma (BCL-2) family member BCL-2 adenovirus E1B 19 kDa-interacting protein 3 (BNIP3) is linked to mitochondrial targeting after homodimerization, where it functions in inner membrane depolarization and permeabilization of the mitochondrial outer membrane (MOM) mediating cell death. We investigated the basal distribution of cardiac BNIP3 in vivo and its physical interaction with the pro-death protein BCL2 associated X, apoptosis regulator (BAX) and with mitochondria using immunoblot analysis, co-immunoprecipitation, and continuous wave and pulsed electron paramagnetic resonance spectroscopy techniques...
March 23, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28328748/cyclophilin-d-modulates-the-cardiac-mitochondrial-target-of-isoflurane-sevoflurane-and-desflurane
#3
Rania Harisseh, Pascal Chiari, Camille Villedieu, Pauline Sueur, Maryline Abrial, Jean-Luc Fellahi, Michel Ovize, Abdallah Gharib
BACKGROUND: Volatile anesthetics are known to limit myocardial ischemia-reperfusion injuries. Mitochondria were shown to be major contributors to cardioprotection. Cyclophilin D (CypD) is one of the main regulators of mitochondria-induced cell death. We compared the effect of isoflurane, sevoflurane and desflurane in the presence or absence of CypD, to clarify its role in the mechanism of cardioprotection induced by these anesthetics. METHODS: Oxidative phosphorylation, mitochondrial membrane potential and H2O2 production were measured in isolated mitochondria from wild-type or CypD knockout mice in basal conditions and after hypoxia-reoxygenation in presence or absence of volatiles anesthetics...
March 17, 2017: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28325789/sex-specific-differences-in-mitochondria-biogenesis-morphology-respiratory-function-and-ros-homeostasis-in-young-mouse-heart-and-brain
#4
Abdel Rahman M Khalifa, Engy A Abdel-Rahman, Ali M Mahmoud, Mohamed H Ali, Maha Noureldin, Saber H Saber, Mahmoud Mohsen, Sameh S Ali
Sex-specific differences in mitochondrial function and free radical homeostasis are reported in the context of aging but not well-established in pathogeneses occurring early in life. Here, we examine if sex disparity in mitochondria function, morphology, and redox status starts early and hence can be implicated in sexual dimorphism in cardiac as well as neurological disorders prevalent at young age. Although mitochondrial activity in the heart did not significantly vary between sexes, female brain exhibited enhanced respiration and higher reserve capacity...
March 2017: Physiological Reports
https://www.readbyqxmd.com/read/28325213/mitochondrion-a-common-organelle-for-distinct-cell-deaths
#5
Z Wang, C Figueiredo-Pereira, C Oudot, H L A Vieira, C Brenner
Mitochondria are deeply involved in cell fate decisions via their multiple roles in metabolism, cell growth, and cell death. In healthy cells, these functions are highly regulated to provide sufficient energy for cell function, maintain cell homeostasis, and avoid undesirable cell death. This is achieved by an orchestrated cooperation of cellular and molecular mechanisms such as mitochondrial mass control (mitophagy vs biogenesis), oxidative phosphorylation, redox and calcium homeostasis, and the balance between pro- and antiapoptotic proteins...
2017: International Review of Cell and Molecular Biology
https://www.readbyqxmd.com/read/28323531/mitophagy-receptor-fundc1-regulates-mitochondrial-homeostasis-and-protects-the-heart-from-i-r-injury
#6
Weilin Zhang, Sami Siraj, Rong Zhang, Quan Chen
Mitophagy plays pivotal roles in the selective disposal of unwanted mitochondria, and accumulation of damaged mitochondria has been linked to ageing-related diseases. However, definitive proof that mitophagy regulates mitochondrial quality in vivo is lacking. It is also largely unclear whether damaged mitochondria are the cause or just the consequence of these diseases. We previously showed that FUNDC1 is a mitophagy receptor that interacts with LC3 to mediate mitophagy in response to hypoxia in cultured cells...
March 21, 2017: Autophagy
https://www.readbyqxmd.com/read/28303408/methylene-blue-decreases-mitochondrial-lysine-acetylation-in-the-diabetic-heart
#7
Jessica M Berthiaume, Chia-Heng Hsiung, Alison B Austin, Sean P McBrayer, Mikayla M Depuydt, Margaret P Chandler, Masaru Miyagi, Mariana G Rosca
Diabetic cardiomyopathy is preceded by mitochondrial alterations, and progresses to heart failure. We studied whether treatment with methylene blue (MB), a compound that was reported to serve as an alternate electron carrier within the mitochondrial electron transport chain (ETC), improves mitochondrial metabolism and cardiac function in type 1 diabetes. MB was administered at 10 mg/kg/day to control and diabetic rats. Both echocardiography and hemodynamic studies were performed to assess cardiac function...
March 16, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28302481/metformin-improves-cardiac-function-in-mice-with-heart-failure-after-myocardial-infarction-by-regulating-mitochondrial-energy-metabolism
#8
Dan Sun, Fei Yang
To investigate whether metformin can improve the cardiac function through improving the mitochondrial function in model of heart failure after myocardial infarction. Male C57/BL6 mice aged about 8 weeks were selected and the anterior descending branch was ligatured to establish the heart failure model after myocardial infarction. The cardiac function was evaluated via ultrasound after 3 days to determine the modeling was successful, and the mice were randomly divided into two groups. Saline group (Saline) received the intragastric administration of normal saline for 4 weeks, and metformin group (Met) received the intragastric administration of metformin for 4 weeks...
March 14, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28292971/selective-replacement-of-mitochondrial-dna-increases-cardioprotective-effect-of-chronic-continuous-hypoxia-in-spontaneously-hypertensive-rats
#9
Jan Neckar, Anna Svatonova, Romana Weissova, Zdenek Drahota, Pavlina Zajickova, Iveta Brabcova, David Kolar, Petra Alanova, Jana Vasinova, Jan Silhavy, Marketa Hlavackova, Katerina Tauchmannova, Marie Milerova, Bohuslav Ostadal, Ludek Cervenka, Jitka Zurmanova, Martin Kalous, Olga Novakova, Jiri Novotny, Michal Pravenec, Frantisek Kolar
Mitochondria play an essential role in improved cardiac ischemic tolerance conferred by adaptation to chronic hypoxia. In the present study, we analyzed effects of continuous normobaric hypoxia (CNH) on mitochondrial functions, including the sensitivity of mitochondrial permeability transition pore (MPTP) to opening, and infarct size in hearts of spontaneously hypertensive rats (SHR) and in conplastic SHR-mtBN strain characterized by the selective replacement of the mitochondrial genome of SHR with that of more ischemia-resistant Brown Norway (BN) strain...
March 14, 2017: Clinical Science (1979-)
https://www.readbyqxmd.com/read/28292968/micu1-alleviates-diabetic-cardiomyopathy-through-mitochondrial-ca-2-dependent-antioxidant-response
#10
Lele Ji, Fengzhou Liu, Zhe Jing, Qichao Huang, Ya Zhao, Haiyan Cao, Jun Li, Chun Yin, Jinliang Xing, Fei Li
Diabetic cardiomyopathy is a major cause of mortality in diabetic patients, but specific strategies for prevention or treatment of diabetic cardiomyopathy have not been clarified yet. MICU1 is a key regulator of mitochondria Ca(2+) uptake, which plays important roles in regulating mitochondrial oxidative phosphorylation and redox balance. However, to date, the significance of MICU1 in diabetic hearts has never been investigated. Here, we demonstrated that MICU1 was downregulated in db/db mouse heart, which contributes to myocardial apoptosis in diabetes...
March 14, 2017: Diabetes
https://www.readbyqxmd.com/read/28288978/mff-dependent-mitochondrial-fission-contributes-to-the-pathogenesis-of-cardiac-microvasculature-ischemia-reperfusion-injury-via-induction-of-mros-mediated-cardiolipin-oxidation-and-hk2-vdac1-disassociation-involved-mptp-opening
#11
Hao Zhou, Shunying Hu, Qinhua Jin, Chen Shi, Ying Zhang, Pingjun Zhu, Qiang Ma, Feng Tian, Yundai Chen
BACKGROUND: The cardiac microvascular system ischemia/reperfusion injury following percutaneous coronary intervention is a clinical thorny problem. This study explores the mechanisms by which ischemia/reperfusion injury induces cardiac microcirculation collapse. METHODS AND RESULTS: In wild-type mice, mitochondrial fission factor (Mff) expression increased in response to acute microvascular ischemia/reperfusion injury. Compared with wild-type mice, homozygous Mff-deficient (Mff(gt)) mice exhibited a smaller infarcted area, restored cardiac function, improved blood flow, and reduced microcirculation perfusion defects...
March 13, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28275246/sarcoplasmic-reticulum-mitochondria-communication-in-cardiovascular-pathophysiology
#12
REVIEW
Camila Lopez-Crisosto, Christian Pennanen, Cesar Vasquez-Trincado, Pablo E Morales, Roberto Bravo-Sagua, Andrew F G Quest, Mario Chiong, Sergio Lavandero
Repetitive, calcium-mediated contractile activity renders cardiomyocytes critically dependent on a sustained energy supply and adequate calcium buffering, both of which are provided by mitochondria. Moreover, in vascular smooth muscle cells, mitochondrial metabolism modulates cell growth and proliferation, whereas cytosolic calcium levels regulate the arterial vascular tone. Physical and functional communication between mitochondria and sarco/endoplasmic reticulum and balanced mitochondrial dynamics seem to have a critical role for optimal calcium transfer to mitochondria, which is crucial in calcium homeostasis and mitochondrial metabolism in both types of muscle cells...
March 9, 2017: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/28272306/akt2-blocks-nucleus-translocation-of-apoptosis-inducing-factor-aif-and-endonuclease-g-endog-while-promoting-caspase-activation-during-cardiac-ischemia
#13
Shuai Yang, Xinmei Zhao, Hui Xu, Fan Chen, Yitao Xu, Zhe Li, Daniel Sanchis, Liang Jin, Yubin Zhang, Junmei Ye
The AKT (protein kinase B, PKB) family has been shown to participate in diverse cellular processes, including apoptosis. Previous studies demonstrated that protein kinase B2 (AKT2(-/-)) mice heart was sensitized to apoptosis in response to ischemic injury. However, little is known about the mechanism and apoptotic signaling pathway. Here, we show that AKT2 inhibition does not affect the development of cardiomyocytes but increases cell death during cardiomyocyte ischemia. Caspase-dependent apoptosis of both the extrinsic and intrinsic pathway was inactivated in cardiomyocytes with AKT2 inhibition during ischemia, while significant mitochondrial disruption was observed as well as intracytosolic translocation of cytochrome C (Cyto C) together with apoptosis-inducing factor (AIF) and endonuclease G (EndoG), both of which are proven to conduct DNA degradation in a range of cell death stimuli...
March 6, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28258543/reducing-mitochondrial-bound-hexokinase-ii-mediates-transition-from-non-injurious-into-injurious-ischemia-reperfusion-of-the-intact-heart
#14
Rianne Nederlof, Ebru Gürel-Gurevin, Otto Eerbeek, Chaoqin Xie, G Sjoerd Deijs, Moritz Konkel, Jun Hu, Nina C Weber, Cees A Schumacher, Antonius Baartscheer, Egbert G Mik, Markus W Hollmann, Fadi G Akar, Coert J Zuurbier
Ischemia/reperfusion (I/R) of the heart becomes injurious when duration of the ischemic insult exceeds a certain threshold (approximately ≥20 min). Mitochondrial bound hexokinase II (mtHKII) protects against I/R injury, with the amount of mtHKII correlating with injury. Here, we examine whether mtHKII can induce the transition from non-injurious to injurious I/R, by detaching HKII from mitochondria during a non-injurious I/R interval. Additionally, we examine possible underlying mechanisms (increased reactive oxygen species (ROS), increased oxygen consumption (MVO2) and decreased cardiac energetics) associated with this transition...
March 3, 2017: Journal of Physiology and Biochemistry
https://www.readbyqxmd.com/read/28249782/aldh2-restores-exhaustive-exercise-induced-mitochondrial-dysfunction-in-skeletal-muscle
#15
Qiuping Zhang, Jianheng Zheng, Jun Qiu, Xiahong Wu, Yangshuo Xu, Weili Shen, Mengwei Sun
BACKGROUND: Mitochondrial aldehyde dehydrogenase 2 (ALDH2) is highly expressed in heart and skeletal muscles, and is the major enzyme that metabolizes acetaldehyde and toxic aldehydes. The cardioprotective effects of ALDH2 during cardiac ischemia/reperfusion injury have been recognized. However, less is known about the function of ALDH2 in skeletal muscle. This study was designed to evaluate the effect of ALDH2 on exhaustive exercise-induced skeletal muscle injury. METHODS: We created transgenic mice expressing ALDH2 in skeletal muscles...
April 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28237394/developmental-changes-in-the-balance-of-glycolytic-atp-production-and-oxidative-phosphorylation-in-ventricular-cells-a-simulation-study
#16
Hitomi I Sano, Tamami Toki, Yasuhiro Naito, Masaru Tomita
The developmental program of the heart requires accurate regulation to ensure continuous circulation and simultaneous cardiac morphogenesis, because any functional abnormalities may progress to congenital heart malformation. Notably, energy metabolism in fetal ventricular cells is regulated in a manner that differs from adult ventricular cells: fetal cardiomyocytes generally have immature mitochondria and fetal ventricular cells show greater dependence on glycolytic ATP production. However, although various characteristics of energy metabolism in fetal ventricular cells have been reported, to our knowledge, a quantitative description of the contributions of these factors to fetal ventricular cell functions has not yet been established...
February 24, 2017: Journal of Theoretical Biology
https://www.readbyqxmd.com/read/28231026/late-administration-of-a-palladium-lipoic-acid-complex-poly-mva-modifies-cardiac-mitochondria-but-not-functional-or-structural-manifestations-of-radiation-induced-heart-disease-in-a-rat-model
#17
Vijayalakshmi Sridharan, John W Seawright, Francis J Antonawich, Merrill Garnett, Maohua Cao, Preeti Singh, Marjan Boerma
Exposure of the heart to ionizing radiation can cause adverse myocardial remodeling. In small animal models, local heart irradiation causes persistent alterations in cardiac mitochondrial function and swelling. POLY-MVA is a dietary supplement that contains a palladium lipoic acid complex that targets mitochondrial complex I and has been demonstrated to have greater redox potential than lipoic acid alone. POLY-MVA improves mitochondrial function and anti-oxidant enzyme activity in the aged rat heart. In this study, we tested whether POLY-MVA can mitigate cardiac effects of ionizing radiation...
February 23, 2017: Radiation Research
https://www.readbyqxmd.com/read/28219828/treating-cognitive-impairment-with-transcranial-low-level-laser-therapy
#18
Jack C de la Torre
This report examines the potential of low level laser therapy (LLLT) to alter brain cell function and neurometabolic pathways using red or near infrared (NIR) wavelengths transcranially for the prevention and treatment of cognitive impairment. Although laser therapy on human tissue has been used for a number of medical conditions since the late 1960s, it is only recently that several clinical studies have shown its value in raising neurometabolic energy levels that can improve cerebral hemodynamics and cognitive abilities in humans...
February 13, 2017: Journal of Photochemistry and Photobiology. B, Biology
https://www.readbyqxmd.com/read/28216385/the-role-of-mitochondria-in-cardiac-development-and-protection
#19
REVIEW
Jaakko L Pohjoismäki, Steffi Goffart
Mitochondria are essential for the development as well as maintenance of the myocardium, the most energy consuming tissue in the human body. Mitochondria are not only a source of ATP energy but also generators of reactive oxygen species (ROS), that cause oxidative damage, but also regulate physiological processes such as the switch from hyperplastic to hypertrophic growth after birth. As excess ROS production and oxidative damage are associated with cardiac pathology, it is not surprising that much of the research focused on the deleterious aspects of free radicals...
February 17, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28205173/measurement-of-mitochondrial-cholesterol-import-using-a-mitochondria-targeted-cyp11a1-fusion-construct
#20
Barry E Kennedy, Mark Charman, Barbara Karten
All animal membranes require cholesterol as an essential regulator of biophysical properties and function, but the levels of cholesterol vary widely among different subcellular compartments. Mitochondria, and in particular the inner mitochondrial membrane, have the lowest levels of cholesterol in the cell. Nevertheless, mitochondria need cholesterol for membrane maintenance and biogenesis, as well as oxysterol, steroid, and hepatic bile acid production. Alterations in mitochondrial cholesterol have been associated with a range of pathological conditions, including cancer, hepatosteatosis, cardiac ischemia, Alzheimer's, and Niemann-Pick Type C Disease...
2017: Methods in Molecular Biology
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