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mitochondria and heart failure

Xiaolong Xu, Qingquan Liu, Shasha He, Jingxia Zhao, Ning Wang, Xuyang Han, Yuhong Guo
Sepsis is reported to be an unusual systemic reaction to infection, accompanied by multiple-organ failure. Sepsis-induced cardiomyopathy (SIC), defined as damages and dysfunction of the heart, is essential in the pathogenesis of sepsis. Traditional Chinese formula, which has long been used to improve the situation of patients through multitarget regulation, is now gradually being used as complementary therapy. The present study aimed to investigate the effect of Qiang-Xin 1 (QX1) formula, a traditional Chinese herbal medicine designed for cardiac dysfunction, on cecal ligation puncture (CLP)-induced heart damage and its underlying mechanisms in mice...
2018: Frontiers in Pharmacology
Teng Sun, Meng-Yang Li, Pei-Feng Li, Ji-Min Cao
Autophagy, which is an evolutionarily conserved process according to the lysosomal degradation of cellular components, plays a critical role in maintaining cell homeostasis. Autophagy and mitochondria autophagy (mitophagy) contribute to the preservation of cardiac homeostasis in physiological settings. However, impaired or excessive autophagy is related to a variety of diseases. Recently, a close link between autophagy and cardiac disorders, including myocardial infarction, cardiac hypertrophy, cardiomyopathy, cardiac fibrosis, and heart failure, has been demonstrated...
August 11, 2018: Cells
Chih-Yang Huang, Chao-Hung Lai, Chia-Hua Kuo, Shu-Fen Chiang, Pei-Ying Pai, Jing-Ying Lin, Chih-Fen Chang, Vijaya Padma Viswanadha, Wei-Wen Kuo, Chih-Yang Huang
Mitochondrial dysfunction is a major contributor to myocyte loss and the development of heart failure. Myocytes have quality control mechanisms to retain functional mitochondria by removing damaged mitochondria via specialized autophagy, i.e., mitophagy. The underlying mechanisms of fission affect the survival of cardiomyocytes, and left ventricular function in the heart is poorly understood. Here, we demonstrated the direct effect and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in heart failure...
August 9, 2018: Journal of Molecular and Cellular Cardiology
Celal Guven
Cardiac hypertrophy is associated with mitochondrial dysfunctions, which leads to heart failure if sustained. The aim of present study is to test hypothesis whether activation of mitochondrial KATP channel (mitoKATP) by diazoxide improve mitochondrial membrane potential (MMP) and oxidative stress in an in vitro model of cardiac hypertrophy. Rat cardiomyocytes cell line (H9c2) was used to create four groups as control, diazoxide, hypertrophy, hypertrophy and diazoxide. Norepinephrine was used to induce hypertrophy...
July 30, 2018: Cellular and Molecular Biology
Cheng-Hsien Chou, Tieh-Cheng Fu, Hsing-Hua Tsai, Chih-Chin Hsu, Chao-Hung Wang, Jong-Shyan Wang
OBJECTIVE: Exercise improves cardiopulmonary fitness and reduces the risk of vascular thrombosis in patients with cardiovascular diseases. In platelets, mitochondria carry out cellular bioenergetics and thrombogenesis. This study aimed to elucidate the effect of high-intensity interval training (HIIT) on systemic aerobic capacity and platelet mitochondrial bioenergetics in patients with heart failure (HF). METHODS: Thirty-four randomly selected HF patients engaged in HIIT (3-min intervals at 40% and 80% of VO2peak , n = 17) for 30 min/day, 3 days/week for 12 weeks, or to a control group that received general healthcare (GHC; n = 17)...
July 27, 2018: International Journal of Cardiology
Ryan J Pewowaruk, Jennifer L Philip, Shivendra G Tewari, Claire S Chen, Mark S Nyaeme, Zhijie Wang, Diana M Tabima, Anthony J Baker, Daniel A Beard, Naomi C Chesler
Right ventricular (RV) failure, which occurs in the setting of pressure overload, is characterized by abnormalities in mechanical and energetic function. The effects of these cell- and tissue-level changes on organ-level RV function are unknown. The primary aim of this study was to investigate the effects of myofiber mechanics and mitochondrial energetics on organ-level RV function in the context of pressure overload using a multiscale model of the cardiovascular system. The model integrates the mitochondria-generated metabolite concentrations that drive intracellular actin-myosin cross-bridging and extracellular myocardial tissue mechanics in a biventricular heart model coupled with simple lumped parameter circulations...
August 1, 2018: Journal of Biomechanical Engineering
Karolina E Hilse, Anne Rupprecht, Monika Egerbacher, Sarah Bardakji, Lars Zimmermann, Andrea E M Seiler Wulczyn, Elena E Pohl
The involvement of mitochondrial uncoupling proteins 2 and 3 in the pathogenesis of cardiovascular diseases is widely acknowledged. However, contradictory reports show that the functions of UCP2/UCP3 are still disputed. We have previously described that UCP2 is highly abundant in cells that rely on glycolysis, such as stem, cancer and activated immune cells. In contrast, high amounts of UCP3 are present in brown adipose tissue, followed by heart and skeletal muscles - all known to metabolize fatty acids (FA) to a high extent...
2018: Frontiers in Physiology
Shafiul Alam, Chowdhury S Abdullah, Richa Aishwarya, Sumitra Miriyala, Manikandan Panchatcharam, Jonette M Peretik, A Wayne Orr, Jeanne James, Jeffrey Robbins, Md Shenuarin Bhuiyan
BACKGROUND: Desmin filament proteins interlink the contractile myofibrillar apparatus with mitochondria, nuclei and the sarcolemma. Mutations in the human desmin gene cause cardiac disease, remodeling, and heart failure but the pathophysiological mechanisms remain unknown. METHODS AND RESULTS: Cardiomyocyte-specific overexpression of mutated desmin (a 7 amino acid deletion R172-E178, D7-Des Tg) causes accumulations of electron-dense aggregates and myofibrillar degeneration associated with cardiac dysfunction...
July 9, 2018: Journal of the American Heart Association
Yoshitake Cho, Robert S Ross
Immobilization, bed rest, or denervation leads to muscle disuse and subsequent skeletal muscle atrophy. Muscle atrophy can also occur as a component of various chronic diseases such as cancer, AIDS, sepsis, diabetes, chronic heart failure, or as a direct result of genetic muscle disorders. In addition to this atrophic loss of muscle mass, metabolic deregulation of muscle also occurs. In contrast, physical exercise plays a beneficial role in counteracting disuse-induced atrophy by increasing muscle mass and strength...
June 29, 2018: Physiological Genomics
Cameron S Brand, Valerie P Tan, Joan Heller Brown, Shigeki Miyamoto
Cardiac ischemia/reperfusion, loss of blood flow and its subsequent restoration, causes damage to the heart. Oxidative stress from ischemia/reperfusion leads to dysfunction and death of cardiomyocytes, increasing the risk of progression to heart failure. Alterations in mitochondrial dynamics, in particular mitochondrial fission, have been suggested to play a role in cardioprotection from oxidative stress. We tested the hypothesis that activation of RhoA regulates mitochondrial fission in cardiomyocytes. Our studies show that expression of constitutively active RhoA in cardiomyocytes increases phosphorylation of Dynamin-related protein 1 (Drp1) at serine-616, and leads to localization of Drp1 at mitochondria...
October 2018: Cellular Signalling
Masashi Mizuno, Atsushi Kuno, Toshiyuki Yano, Takayuki Miki, Hiroto Oshima, Tatsuya Sato, Kei Nakata, Yukishige Kimura, Masaya Tanno, Tetsuji Miura
To explore mechanisms by which SGLT2 inhibitors protect diabetic hearts from heart failure, we examined the effect of empagliflozin (Empa) on the ultrastructure of cardiomyocytes in the noninfarcted region of the diabetic heart after myocardial infarction (MI). OLETF, a rat model of type 2 diabetes, and its nondiabetic control, LETO, received a sham operation or left coronary artery ligation 12 h before tissue sampling. Tissues were sampled from the posterior ventricle (i.e., the remote noninfarcted region in rats with MI)...
June 2018: Physiological Reports
Jung Hyun Park, Hyeong Jun Ku, Jae Kyeom Kim, Jeen-Woo Park, Jin Hyup Lee
Heart failure is a frequent unfavorable outcome of pathological cardiac hypertrophy. Recent increase in dietary fructose consumption mirrors the rise in prevalence of cardiovascular diseases such as cardiac hypertrophy leading to concerns raised by public health experts. Mitochondria, comprising 30% of cardiomyocyte volume, play a central role in modulating redox-dependent cellular processes such as metabolism and apoptosis. Furthermore, mitochondrial dysfunction is a key cause of pathogenesis of fructose-induced cardiac hypertrophy...
June 21, 2018: Scientific Reports
T Dung Nguyen, Michael Schwarzer, Andrea Schrepper, Paulo A Amorim, Daniel Blum, Claudia Hain, Gloria Faerber, Judith Haendeler, Joachim Altschmied, Torsten Doenst
BACKGROUND: Insulin resistance in diabetes mellitus has been associated with mitochondrial dysfunction. Defects at the level of mitochondria are also characteristic of heart failure. We assessed changes in cardiac insulin response and mitochondrial function in a model of pressure overload-induced heart failure. METHODS AND RESULTS: Rats underwent aortic banding to induce pressure overload. At 10 weeks, rats showed cardiac hypertrophy and pulmonary congestion, but left ventricular dilatation and systolic dysfunction were only evident after 20 weeks...
June 21, 2018: Journal of the American Heart Association
Salvador Meseguer, Joaquin Panadero, Carmen Navarro-González, Magda Villarroya, Rachid Boutoual, Giacomo Pietro Comi, M-Eugenia Armengod
The pathomechanisms underlying oxidative phosphorylation (OXPHOS) diseases are not well-understood, but they involve maladaptive changes in mitochondria-nucleus communication. Many studies on the mitochondria-nucleus cross-talk triggered by mitochondrial dysfunction have focused on the role played by regulatory proteins, while the participation of miRNAs remains poorly explored. MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is mostly caused by mutation m.3243A>G in mitochondrial tRNALeu(UUR) gene...
September 2018: Biochimica et Biophysica Acta
Edoardo Bertero, Christoph Maack
The heart consumes large amounts of energy in the form of ATP that is continuously replenished by oxidative phosphorylation in mitochondria and, to a lesser extent, by glycolysis. To adapt the ATP supply efficiently to the constantly varying demand of cardiac myocytes, a complex network of enzymatic and signalling pathways controls the metabolic flux of substrates towards their oxidation in mitochondria. In patients with heart failure, derangements of substrate utilization and intermediate metabolism, an energetic deficit, and oxidative stress are thought to underlie contractile dysfunction and the progression of the disease...
June 18, 2018: Nature Reviews. Cardiology
Swati Dey, Deeptankar DeMazumder, Agnieszka Sidor, D Brian Foster, Brian O'Rourke
RATIONALE: Despite increasing prevalence and incidence of heart failure (HF), therapeutic options remain limited. In early stages of HF, sudden cardiac death (SCD) from ventricular arrhythmias claims many lives. Reactive oxygen species (ROS) have been implicated in both arrhythmias and contractile dysfunction. However, little is known about how ROS in specific subcellular compartments contribute to HF or SCD pathophysiology. The role of ROS in chronic proteome remodeling has not been explored...
July 20, 2018: Circulation Research
Irina Odinokova, Yulia Baburina, Alexey Kruglov, Irina Fadeeva, Alena Zvyagina, Linda Sotnikova, Vladimir Akatov, Olga Krestinina
Excessive generation of reactive oxygen species (ROS) in mitochondria and the opening of the nonselective mitochondrial permeability transition pore are important factors that promote cardiac pathologies and dysfunction. The hormone melatonin (MEL) is known to improve the functional state of mitochondria via an antioxidant effect. Here, the effect of MEL administration on heart mitochondria from aged rats with acute cardiac failure caused by isoprenaline hydrochloride (ISO) was studied. A histological analysis revealed that chronic intake of MEL diminished the age-dependent changes in the structure of muscle fibers of the left ventricle, muscle fiber swelling, and injury zones characteristic of acute cardiac failure caused by ISO...
May 23, 2018: International Journal of Molecular Sciences
Junxia Zhang, Dairu Liu, Mao Zhang, Yan Zhang
Excessive death of cardiac myocytes leads to many cardiac diseases, including myocardial infarction, arrhythmia, heart failure and sudden cardiac death. For the last several decades, most work on cell death has focused on apoptosis, which is generally considered as the only form of regulated cell death, whereas necrosis has been regarded to be an unregulated process. Recent findings reveal that necrosis also occurs in a regulated manner and that it is closely related to the physiology and pathophysiology of many organs, including the heart...
May 18, 2018: British Journal of Pharmacology
Edoardo Bertero, Christoph Maack
In heart failure, alterations of Na+ and Ca2+ handling, energetic deficit, and oxidative stress in cardiac myocytes are important pathophysiological hallmarks. Mitochondria are central to these processes because they are the main source for ATP, but also reactive oxygen species (ROS), and their function is critically controlled by Ca2+ During physiological variations of workload, mitochondrial Ca2+ uptake is required to match energy supply to demand but also to keep the antioxidative capacity in a reduced state to prevent excessive emission of ROS...
May 11, 2018: Circulation Research
Wei Li, David Kennedy, Zhili Shao, Xi Wang, Andre Klaassen Kamdar, Malory Weber, Kayla Mislick, Kathryn Kiefer, Rommel Morales, Brendan Agatisa-Boyle, Diana M Shih, Srinivasa T Reddy, Christine S Moravec, W H Wilson Tang
BACKGROUND: Mitochondrial oxidation is a major source of reactive oxygen species (ROS) and mitochondrial dysfunction plays a central role in development of heart failure (HF). Paraoxonase 2 deficient (PON2-def) mitochondria are impaired in function. In this study, we tested whether PON2-def aggravates HF progression. METHODS AND RESULTS: Using qPCR, immunoblotting and lactonase activity assay, we demonstrate that PON2 activity was significantly decreased in failing hearts despite increased PON2 expression...
June 2018: Free Radical Biology & Medicine
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