keyword
MENU ▼
Read by QxMD icon Read
search

mitochondria and cardiovascular disease

keyword
https://www.readbyqxmd.com/read/27911307/a-high-cholesterol-diet-increases-27-hydroxycholesterol-and-modifies-estrogen-receptor-expression-and-neurodegeneration-in-rabbit-hippocampus
#1
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
#2
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...
November 24, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27844171/mitochondrial-dynamics-as-a-therapeutic-target-for-treating-cardiac-diseases
#3
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
#4
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 9, 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
#5
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...
November 1, 2016: Environmental Pollution
https://www.readbyqxmd.com/read/27814605/linking-telomere-loss-and-mitochondrial-dysfunction-in-chronic-disease
#6
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)
https://www.readbyqxmd.com/read/27783269/anion-channels-of-mitochondria
#7
Devasena Ponnalagu, Harpreet Singh
Mitochondria are the "power house" of a cell continuously generating ATP to ensure its proper functioning. The constant production of ATP via oxidative phosphorylation demands a large electrochemical force that drives protons across the highly selective and low-permeable mitochondrial inner membrane. Besides the conventional role of generating ATP, mitochondria also play an active role in calcium signaling, generation of reactive oxygen species (ROS), stress responses, and regulation of cell-death pathways...
October 26, 2016: Handbook of Experimental Pharmacology
https://www.readbyqxmd.com/read/27779647/asiatic-acid-inhibits-lactate-induced-cardiomyocyte-apoptosis-through-the-regulation-of-the-lactate-signaling-cascade
#8
Changzheng Gao, Fen Wang, Zhiqiang Wang, Jing Zhang, Xiangjun Yang
The lactate signaling cascade has recently been linked to mitochondrial energy metabolism and cardiomyocyte apoptosis in several cardiovascular diseases. Asiatic acid (AA) exhibits a variety of pharmacological effects, including antioxidant and anti-apoptotic effects. In this study, we investigated the protective effects of AA against the lactate-induced apoptosis of cardiomyocytes, as well as its mechanisms of action. Neonatal rat cardiomyocytes were pre-treated with 20 µM AA for 24 h, followed by exposure to 20 mM lactate for a further 24 h...
October 20, 2016: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/27774507/reactive-oxygen-species-a-key-hallmark-of-cardiovascular-disease
#9
Nisha Panth, Keshav Raj Paudel, Kalpana Parajuli
Cardiovascular diseases (CVDs) have been the prime cause of mortality worldwide for decades. However, the underlying mechanism of their pathogenesis is not fully clear yet. It has been already established that reactive oxygen species (ROS) play a vital role in the progression of CVDs. ROS are chemically unstable reactive free radicals containing oxygen, normally produced by xanthine oxidase, nicotinamide adenine dinucleotide phosphate oxidase, lipoxygenases, or mitochondria or due to the uncoupling of nitric oxide synthase in vascular cells...
2016: Advances in Medicine
https://www.readbyqxmd.com/read/27758700/mutations-of-nuclear-and-mitochondrial-genomes-as-potential-targets-for-the-treatment-of-metabolic-syndrome
#10
Elena V Galitsyna, Andrey V Zhelankin, Igor A Sobenin, Alexander N Orekhov
In addition to external factors, such as exercise, food and the environment, genetic predisposition makes great contribution to the development of metabolic disorders and cardiovascular disease. This review is aimed to examine the genetic basis of complex metabolic disorders conventionally described as "metabolic syndrome" (MetS), with the special focus on currently known mutations in the nuclear and mitochondrial genomes, which are associated both with the individual components of MetS and combinations thereof, and also on the studies of the relationship of MetS phenotype as a binary trait...
October 18, 2016: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/27746034/role-of-oxidative-stress-and-antioxidants-in-daily-nutrition-and-human-health
#11
REVIEW
Geir Bjørklund, Salvatore Chirumbolo
Diet may be defined as a complex process that should involve a deeper comprehension of metabolism, energy balance, and the molecular pathways involved in cellular stress response and survival, gut microflora genetics, enzymatic polymorphism within the human population, and the role of plant-derived polyphenols in this context. Metabolic syndrome, encompassing pathologies with a relatively high morbidity, such as type 2 diabetes, obesity, and cardiovascular disease, is a bullet point of the big concern about how daily dietary habits should promote health and prevent metabolic impairments to prevent hospitalization and the need for health care...
January 2017: Nutrition
https://www.readbyqxmd.com/read/27740971/resolution-of-mitochondrial-oxidant-stress-improves-aged-cardiovascular-performance
#12
Takashi Owada, Hiroyuki Yamauchi, Shu-Ichi Saitoh, Shunsuke Miura, Hirofumi Machii, Yasuchika Takeishi
BACKGROUND: Senescence is a major factor that increases oxidative stress in mitochondria, which contributes toward the pathogenesis of heart disease. However, the effect of antioxidant therapy on cardiac mitochondria in aged-cardiac performance remains elusive. OBJECTIVES: We postulated that the mitochondrial targeting of superoxide scavenging would have benefits in the aged heart. METHODS AND RESULTS: Generation of superoxide in the mitochondria and nicotinamide adenine dinucleotide phosphate oxidase activity increased in the heart of old mice compared with that in young mice...
October 12, 2016: Coronary Artery Disease
https://www.readbyqxmd.com/read/27738100/novel-compounds-targeting-the-mitochondrial-protein-vdac1-inhibit-apoptosis-and-protect-against-mitochondrial-dysfunction
#13
Danya Ben-Hail, Racheli Begas-Shvartz, Moran Shalev, Anna Shteinfer-Kuzmine, Arie Gruzman, Simona Reina, Vito De Pinto, Varda Shoshan-Barmatz
Apoptosis is thought to play a critical role in several pathological processes, such as neurodegenerative diseases (i.e. Parkinson's and Alzheimer's diseases) and various cardiovascular diseases. Despite the fact that apoptotic mechanisms are well defined, there is still no substantial therapeutic strategy to stop or even slow this process. Thus, there is an unmet need for therapeutic agents that are able to block or slow apoptosis in neurodegenerative and cardiovascular diseases. The outer mitochondrial membrane protein voltage-dependent anion channel 1 (VDAC1) is a convergence point for a variety of cell survival and death signals, including apoptosis...
November 25, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27737949/metformin-suppresses-diabetes-accelerated-atherosclerosis-via-the-inhibition-of-drp1-mediated-mitochondrial-fission
#14
Qilong Wang, Miao Zhang, Gloria Torres, Shengnan Wu, Changhan Ouyang, Zhonglin Xie, Ming-Hui Zou
Metformin is a widely used anti-diabetic drug that exerts cardiovascular protective effects in patients with diabetes. How metformin protects diabetes-related cardiovascular diseases remains poorly understood. Here, we show that metformin abated the progression of diabetes-accelerated atherosclerosis by inhibiting mitochondrial fission in endothelial cells.Metformin treatments markedly reduced mitochondrial fragmentation, mitigated mitochondrial-derived superoxide release, improved endothelial-dependent vasodilation, inhibited vascular inflammation, and suppressed atherosclerotic lesions in streptozotocin (STZ)-induced diabetic ApoE(-/-) mice...
October 13, 2016: Diabetes
https://www.readbyqxmd.com/read/27735003/mito-magneto-a-tool-for-nanoparticle-mediated-mitochondria-isolation
#15
Bhabatosh Banik, Brett W Askins, Shanta Dhar
The field of intracellular organelle targeting using nanoparticle (NP) is mushrooming rapidly. Thus, the area of nanotechnology-enabled targeting of mitochondrion, the cellular powerhouse, for diseases characterized by mitochondrial dysfunctions such as cancer, diseases of the central nervous system, and cardiovascular diseases is also growing at a rapid pace. Optimization of a NP's ability to target the mitochondria requires quantification of the particles in this subcellular organelle and isolation of mitochondria from the cells...
December 1, 2016: Nanoscale
https://www.readbyqxmd.com/read/27704213/network-analysis-of-mitonuclear-gwas-reveals-functional-networks-and-tissue-expression-profiles-of-disease-associated-genes
#16
Simon C Johnson, Brenda Gonzalez, Quanwei Zhang, Brandon Milholland, Zhengdong Zhang, Yousin Suh
While mitochondria have been linked to many human diseases through genetic association and functional studies, the precise role of mitochondria in specific pathologies, such as cardiovascular, neurodegenerative, and metabolic diseases, is often unclear. Here, we take advantage of the catalog of human genome-wide associations, whole-genome tissue expression and expression quantitative trait loci datasets, and annotated mitochondrial proteome databases to examine the role of common genetic variation in mitonuclear genes in human disease...
October 4, 2016: Human Genetics
https://www.readbyqxmd.com/read/27679744/critical-role-of-mitochondrial-ros-is-dependent-on-their-site-of-production-on-the-electron-transport-chain-in-ischemic-heart
#17
Ngonidzashe B Madungwe, Netanel F Zilberstein, Yansheng Feng, Jean C Bopassa
Reactive oxygen species (ROS) generation has been implicated in many pathologies including ischemia/reperfusion (I/R) injury. This led to multiple studies on antioxidant therapies to treat cardiovascular diseases but paradoxically, results have so far been mixed as ROS production can be beneficial as a signaling mechanism and in cardiac protection via preconditioning interventions. We investigated whether the differential impact of increased ROS in injury as well as in protection could be explained by their site of production on the mitochondrial electron transport chain...
2016: American Journal of Cardiovascular Disease
https://www.readbyqxmd.com/read/27649969/epac2-rap1-signaling-regulates-reactive-oxygen-species-production-and-susceptibility-to-cardiac-arrhythmias
#18
Zhaokang Yang, Hannah Kirton, Moza Al-Owais, Jerôme Thireau, Sylvain Richard, Derek Steele, Chris Peers
AIMS: In the heart, β<sub>1</sub>-adrenergic signaling involves cyclic adenosine monophosphate (cAMP) acting via both protein kinase-A (PKA) and 'exchange protein directly activated by cAMP' (Epac): a guanine nucleotide exchange factor for the small GTPase Rap1. Inhibition of Epac-Rap1 signaling has been proposed as a therapeutic strategy for both cancer and cardiovascular disease. However, previous work suggests that impaired Rap1 signaling may have detrimental effects on cardiac function...
September 21, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27633387/aldehyde-dehydrogenase-2-roles-in-ischemic-cardiovascular-disease
#19
Xiangwei Liu, Aijun Sun
Coronary heart disease is the leading cause of mortality and morbidity, incurring a major burden of medical care. Even with increasing application of emergent recanalization (PCI and CABG) therapy, ischemia and ischemic reperfusion injury remain as the dominant pathological process that damages cardiomyocytes. Mitochondrial Aldehyde dehydrogenase-2 (ALDH2) is a multifunctional enzyme catalyzing the oxidation of aldehydes. Accumulating data have shown that ALDH2 can help restore mitochondria function by eliminating toxic aldehyde and participating in cellular signaling important for cell adaption and survival...
September 12, 2016: Current Drug Targets
https://www.readbyqxmd.com/read/27629697/equine-metabolic-syndrome-impairs-adipose-stem-cells-osteogenic-differentiation-by-predominance-of-autophagy-over-selective-mitophagy
#20
Krzysztof Marycz, Katarzyna Kornicka, Monika Marędziak, Paweł Golonka, Jakub Nicpoń
Adipose-derived mesenchymal stem cells (ASC) hold great promise in the treatment of many disorders including musculoskeletal system, cardiovascular and/or endocrine diseases. However, the cytophysiological condition of cells, used for engraftment seems to be fundamental factor that might determine the effectiveness of clinical therapy. In this study we investigated growth kinetics, senescence, accumulation of oxidative stress factors, mitochondrial biogenesis, autophagy and osteogenic differentiation potential of ASC isolated from horses suffered from equine metabolic syndrome (EMS)...
September 14, 2016: Journal of Cellular and Molecular Medicine
keyword
keyword
117424
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"