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mitochondria and cardiovascular disease

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https://www.readbyqxmd.com/read/28088493/apoptosis-induced-by-the-methanol-extract-of-salvia-miltiorrhiza-bunge-in-non-small-cell-lung-cancer-through-pten-mediated-inhibition-of-pi3k-akt-pathway
#1
Yin-Tao Ye, Wei Zhong, Pei Sun, Dong Wang, Chen Wang, Li-Min Hu, Jun-Qiang Qian
ETHNOPHARMACOLOGICAL RELEVANCE: Salvia miltiorrhiza Bunge, a well-known traditional Chinese medicinal (TCM) plant, has been used to treat cardiovascular diseases since thousands of years. Many studies have reported that the active component tanshinones displayed a variety of biological activities: antithrombous, antiplatelet aggregation, antioxidant and antitumor promoting. But the mechanism of how the active components working still need to be clarified. The anti-tumor effect of compounds of tanshinone (CTN), the methanol extract of Salvia miltiorrhiza Bunge roots, was investigated...
January 11, 2017: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/28078995/sphingolipids-in-genetic-and-acquired-forms-of-chronic-kidney-diseases
#2
Norishi Ueda
Sphingolipids (SLs) regulate apoptosis, proliferation, and stress response. SLs, including ceramide, glycosphingolipids (glucosylceramide, lactosylceramide, and gangliosides) and sphingosine-1-phosphate (S1P), play a role in the pathogenesis and progression of genetic (lysosomal storage disease, congenital nephrotic syndrome and polycystic kidney disease) and non-genetic forms of chronic kidney diseases (CKDs). SLs metabolism defects promote complications (cardiovascular events, etc.) via oxidant stress in CKDs...
January 12, 2017: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/28078981/resilience-to-alzheimer-s-disease-the-role-of-physical-activity
#3
Pedrinolla Anna, Schena Federico, Venturelli Massimo
BACKGROUND: Although Alzheimer's disease (AD) is a neurodegenerative pathology characterized by accumulation of β-amyloid plaques and neurofibrillary tangles at cerebral level, recent studies highlighted that AD might be the result of many altered physiological processes occurring at whole-organism level. The ability to adapt to stressors by "bending" but not "breaking" can be considered as "resilience". Individuals incline to withstand such pathophysiological challenges, can be considered more resilient than those that do not...
January 11, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28051329/regulation-of-the-cardioprotective-adiponectin-and-its-receptor-adipor1-by-salt
#4
Nicholas Arnold, Abuzar Mahmood, Maya Ramdas, Paul P Ehlinger, Lakshmi Pulakat
Both circulating adiponectin (APN) and cardiac APN exert cardioprotective effects and improve insulin sensitivity and mitochondrial function. Low circulating APN serves as a biomarker for cardiovascular risk. Ablation of adiponectin receptor 1 (AdipoR1) causes myocardial mitochondrial dysfunction. Although high salt intake is a contributor to cardiovascular disease, how it modulates the expression of APN or AdipoR1 in cardiomyocytes is not known. We report that APN mRNA expression was attenuated in a dose-dependent manner in mouse cardiomyocyte cell line HL-1 exposed to salt concentrations ranging from 0...
November 30, 2016: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28049038/trimethylamine-n-oxide-impairs-pyruvate-and-fatty-acid-oxidation-in-cardiac-mitochondria
#5
Marina Makrecka-Kuka, Kristine Volska, Unigunde Antone, Reinis Vilskersts, Solveiga Grinberga, Dace Bandere, Edgars Liepinsh, Maija Dambrova
Increased plasma concentration of trimethylamine N-oxide (TMAO), a proatherogenic metabolite, has been linked to adverse cardiovascular outcomes; however, it remains unclear whether TMAO is a biomarker or whether it induces direct detrimental cardiovascular effects. Because altered cardiac energy metabolism and mitochondrial dysfunction play crucial roles in the development of cardiovascular diseases, we hypothesized that increased TMAO concentration may alter mitochondrial energy metabolism. The aim of the present study was to determine the effects of TMAO on cardiac mitochondrial energy metabolism...
December 31, 2016: Toxicology Letters
https://www.readbyqxmd.com/read/28039524/effects-of-cyclic-nucleotide-phosphodiesterases-pdes-on-mitochondrial-skeletal-muscle-functions
#6
REVIEW
Liliane Tetsi, Anne-Laure Charles, Stéphanie Paradis, Anne Lejay, Samy Talha, Bernard Geny, Claire Lugnier
Mitochondria play a critical role in skeletal muscle metabolism and function, notably at the level of tissue respiration, which conduct muscle strength as well as muscle survival. Pathological conditions induce mitochondria dysfunctions notably characterized by free oxygen radical production disturbing intracellular signaling. In that way, the second messengers, cyclic AMP and cyclic GMP, control intracellular signaling at the physiological and transcription levels by governing phosphorylation cascades. Both nucleotides are specifically and selectively hydrolyzed in their respective 5'-nucleotide by cyclic nucleotide phosphodiesterases (PDEs), which constitute a multi-genic family differently tissue distributed and subcellularly compartmentalized...
December 30, 2016: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28034298/effective-agents-targeting-the-mitochondria-and-apoptosis-to-protect-the-heart
#7
Eltyeb Abdelwahid, Aurimas Stulpinas, Audrone Kalvelyte
A wide variety of agents have been traditionally used in cardiovascular medicine worldwide and their precise mechanisms of action have been demonstrated to be largely related to the cardiomyocyte mitochondria and apoptosis. Abnormalities in the structure and function of the mitochondria and mutations in mitochondrial DNA can decrease energy production, alter the redox system, impair calcium homeostasis, and induce the mitochondrial permeability transition pore (MPTP), causing cell death. All of these data provide evidence of mitochondrial signaling pathways as targets to downregulate cardiac cell apoptosis and thus to prevent and treat cardiovascular diseases...
December 29, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/28025032/the-metabolic-syndrome-and-chronic-kidney-disease
#8
REVIEW
Xin Zhang, Lilach O Lerman
The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors including insulin resistance (IR), dyslipidemia, and hypertension, which may also foster development of chronic kidney disease. The mechanisms of MetS-induced kidney disease are not fully understood. The purpose of this review is to summarize recent discoveries regarding the impact of MetS on the kidney, particularly on the renal microvasculature and cellular mitochondria. Fundamental manifestations of MetS include IR and adipose tissue expansion, the latter promoting chronic inflammation and oxidative stress that exacerbate IR...
December 9, 2016: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/28008641/effects-of-mirnas-on-myocardial-apoptosis-by-modulating-mitochondria-related-proteins
#9
REVIEW
Yanfang Zhao, Murugavel Ponnusamy, Yanhan Dong, Lei Zhang, Kun Wang, Peifeng Li
Myocardial apoptosis play a vital role in pathogenesis of cardiovascular diseases. The intrinsic pathway of apoptosis (mitochondrial apoptosis pathway) and abnormal mitochondrial fission and fusion have a detrimental effect on cells under a variety of intracellular stresses including hypoxia, oxidative stress, drug toxicity or DNA damage and contributes to the development of heart failure (HF), myocardial infarction (MI), diabetic cardiomyopathy and ischemia/reperfusion injury (I/R). MicroRNAs (miRNAs) are endogenous short noncoding RNAs, which target 3'-untranslated region of mRNA to switch off gene expression...
December 23, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27995386/the-roles-of-mitochondrial-cation-channels-under-physiological-conditions-and-in-cancer
#10
Ildikò Szabò, Luigi Leanza
Bioenergetics has become central to our understanding of pathological mechanisms as well as the development of new therapeutic strategies and as a tool for gauging disease progression in neurodegeneration, diabetes, cancer, and cardiovascular disease. The view is emerging that inner mitochondrial membrane (IMM) cation channels have a profound effect on mitochondrial function and, consequently, on the metabolic state and survival of the whole cell. Since disruption of the sustained integrity of mitochondria is strongly linked to human disease, pharmacological intervention offers a new perspective concerning neurodegenerative and cardiovascular diseases as well as cancer...
December 20, 2016: Handbook of Experimental Pharmacology
https://www.readbyqxmd.com/read/27995364/transition-in-the-mechanism-of-flow-mediated-dilation-with-aging-and-development-of-coronary-artery-disease
#11
Andreas M Beyer, Natalya Zinkevich, Bradley Miller, Yanping Liu, April L Wittenburg, Michael Mitchell, Ralph Galdieri, Andrey Sorokin, David D Gutterman
In microvessels of patients with coronary artery disease (CAD), flow-mediated dilation (FMD) is largely dependent upon the endothelium-derived hyperpolarizing factor H2O2. The goal of this study is to examine the influence of age and presence or absence of disease on the mechanism of FMD. Human coronary or adipose arterioles (~150 µm diameter) were prepared for videomicroscopy. The effect of inhibiting COX [indomethacin (Indo) or NOS (L-NAME), eliminating H2O2 (polyethylene glycol-catalase (PEG-CAT)] or targeting a reduction in mitochondrial ROS with scavengers/inhibitors [Vitamin E (mtVitamin E); phenylboronic acid (mtPBA)] was determined in children aged 0-18 years; young adults 19-55 years; older adults >55 years without CAD, and similarly aged adults with CAD...
January 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/27982690/mitochondrial-adaptations-in-aged-skeletal-muscle-effect-of-exercise-training
#12
M M Ziaaldini, S Ra Hosseini, M Fathi
The aging process is associated with a decline in mitochondrial functions. Mitochondria dysfunction is involved in initiation and progression of many health problems including neuromuscular, metabolic and cardiovascular diseases. It is well known that endurance exercise improves mitochondrial function, especially in the elderly. However, recent studies have demonstrated that resistance training lead also to substantial increases in mitochondrial function in skeletal muscle. A comprehensive understanding of the cellular mechanisms involved in the skeletal muscle mitochondrial adaptations to exercise training in healthy elderly subjects, can help practitioners to design and prescribe more effective exercise trainings...
December 16, 2016: Physiological Research
https://www.readbyqxmd.com/read/27932069/quercetin-attenuates-vascular-calcification-by-inhibiting-oxidative-stress-and-mitochondrial-fission
#13
Lei Cui, Zhong Li, Xueying Chang, Guangting Cong, Lirong Hao
Vascular calcification is a strong independent predictor of increased cardiovascular morbidity and mortality and has a high prevalence among patients with chronic kidney disease. The present study investigated the effects of quercetin on vascular calcification caused by oxidative stress and abnormal mitochondrial dynamics both in vitro and in vivo. Calcifying vascular smooth muscle cells (VSMCs) treated with inorganic phosphate (Pi) exhibited mitochondrial dysfunction, as demonstrated by decreased mitochondrial potential and ATP production...
December 5, 2016: Vascular Pharmacology
https://www.readbyqxmd.com/read/27919931/low-mt-co1-in-monocytes-and-microvesicles-is-associated-with-outcome-in-patients-with-coronary-artery-disease
#14
Paul Holvoet, Maarten Vanhaverbeke, Katarzyna Bloch, Pieter Baatsen, Peter Sinnaeve, Stefan Janssens
BACKGROUND: Cytochrome oxidase (COX) IV complex regulates energy production in mitochondria. Impaired COX gene expression is related to obesity and type 2 diabetes mellitus, but whether it is directly related to the incidence of cardiovascular events is unknown. We investigated whether COX gene expression in monocytes is predictive for cardiovascular events in coronary artery disease patients. To avoid monocyte isolation from fresh blood, we then aimed to validate our findings in monocyte-derived microvesicles isolated from plasma...
December 5, 2016: Journal of the American Heart Association
https://www.readbyqxmd.com/read/27911307/a-high-cholesterol-diet-increases-27-hydroxycholesterol-and-modifies-estrogen-receptor-expression-and-neurodegeneration-in-rabbit-hippocampus
#15
Sylwia W Brooks, Ava C Dykes, Bernard G Schreurs
Hypercholesterolemia has been implicated in numerous health problems from cardiovascular disease to neurodegeneration. High serum cholesterol levels in midlife have been associated with an increased risk of developing Alzheimer's disease (AD) later in life which suggests that the pathways leading to AD pathology might be activated decades before the symptoms of the disease are detected. Cholesterol-fed animals, particularly cholesterol-fed rabbits, exhibit brain pathology similar to the changes found in brains of AD patients...
November 28, 2016: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/27890624/mitochondrial-camp-prevents-apoptosis-modulating-sirt3-protein-level-and-opa1-processing-in-cardiac-myoblast-cells
#16
Anna Signorile, Arcangela Santeramo, Grazia Tamma, Tommaso Pellegrino, Susanna D'Oria, Paolo Lattanzio, Domenico De Rasmo
Mitochondria, responding to a wide variety of signals, including oxidative stress, are critical in regulating apoptosis that plays a key role in the pathogenesis of a variety of cardiovascular diseases. A number of mitochondrial proteins and pathways have been found to be involved in the mitochondrial dependent apoptosis mechanism, such as optic atrophy 1 (OPA1), sirtuin 3 (Sirt3), deacetylase enzyme and cAMP signal. In the present work we report a network among OPA1, Sirt3 and cAMP in ROS-dependent apoptosis...
February 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27844171/mitochondrial-dynamics-as-a-therapeutic-target-for-treating-cardiac-diseases
#17
Sang-Bing Ong, Derek J Hausenloy
Mitochondria are dynamic in nature and are able to shift their morphology between elongated interconnected mitochondrial networks and a fragmented disconnected arrangement by the processes of mitochondrial fusion and fission, respectively. Changes in mitochondrial morphology are regulated by the mitochondrial fusion proteins - mitofusins 1 and 2 (Mfn1 and 2), and optic atrophy 1 (Opa1) as well as the mitochondrial fission proteins - dynamin-related peptide 1 (Drp1) and fission protein 1 (Fis1). Despite having a unique spatial arrangement, cardiac mitochondria have been implicated in a variety of disorders including ischemia-reperfusion injury (IRI), heart failure, diabetes, and pulmonary hypertension...
November 15, 2016: Handbook of Experimental Pharmacology
https://www.readbyqxmd.com/read/27828948/control-of-mitochondrial-function-and-cell-growth-by-the-atypical-cadherin-fat1
#18
Longyue L Cao, Dario F Riascos-Bernal, Prameladevi Chinnasamy, Charlene M Dunaway, Rong Hou, Mario A Pujato, Brian P O'Rourke, Veronika Miskolci, Liang Guo, Louis Hodgson, Andras Fiser, Nicholas E S Sibinga
Mitochondrial products such as ATP, reactive oxygen species, and aspartate are key regulators of cellular metabolism and growth. Abnormal mitochondrial function compromises integrated growth-related processes such as development and tissue repair, as well as homeostatic mechanisms that counteract ageing and neurodegeneration, cardiovascular disease, and cancer. Physiologic mechanisms that control mitochondrial activity in such settings remain incompletely understood. Here we show that the atypical Fat1 cadherin acts as a molecular 'brake' on mitochondrial respiration that regulates vascular smooth muscle cell (SMC) proliferation after arterial injury...
November 24, 2016: Nature
https://www.readbyqxmd.com/read/27814983/endosulfan-induces-autophagy-and-endothelial-dysfunction-via-the%C3%A2-ampk-mtor-signaling-pathway-triggered-by-oxidative-stress
#19
Lianshuang Zhang, Jialiu Wei, Lihua Ren, Jin Zhang, Ji Wang, Li Jing, Man Yang, Yang Yu, Zhiwei Sun, Xianqing Zhou
Cardiovascular diseases is related to environmental pollution. Endosulfan is an organochlorine pesticide and its toxicity has been reported. However, the relationship between oxidative stress and autophagy induced by endosulfan and its underlying mechanism remain confusing. In this study, human umbilical vein endothelial cells (HUVECs) were chosen to explore the toxicity mechanism and were treated with 0, 1, 6, 12 μg/mL(-1) endosulfan for 24 h, respectively. The present results showed that autophagy could be induced by endosulfan, which was verified by the monodansylcadaverine staining, autophagic ultrastructural observation, and LC3-I/LC3-II conversion...
January 2017: Environmental Pollution
https://www.readbyqxmd.com/read/27814605/linking-telomere-loss-and-mitochondrial-dysfunction-in-chronic-disease
#20
Ana Carlota Gonzales-Ebsen, Niels Gregersen, Rikke Kj Olsen
Telomeres and mitochondria are known to deteriorate over time. Telomere shortening is associated with aging, early senescence, and premature cell death. Mitochondrial dysfunction produces indiscriminate amounts of reactive oxygen species that may lead to oxidative damage to cellular constituents, including telomeric DNA, causing telomere shortening. In fact, primary mitochondrial dysfunction (for example respiratory chain disorders) and secondary mitochondrial dysfunction (such as metabolic diseases, neurodegenerative diseases, cardiovascular diseases, and mood disorders, among others) have been shown to have shorter telomeres than healthy individuals...
January 1, 2017: Frontiers in Bioscience (Landmark Edition)
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