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mitochondria and heart failure

Ting Cao, Shuai Fan, Dong Zheng, Grace Wang, Yong Yu, Ruizhen Chen, Long-Sheng Song, Guo-Chang Fan, Zhuxu Zhang, Tianqing Peng
We and others have reported that calpain-1 was increased in myocardial mitochondria from various animal models of heart disease. This study investigated whether constitutive up-regulation of calpain-1 restricted to mitochondria induced myocardial injury and heart failure and, if so, whether these phenotypes could be rescued by selective inhibition of mitochondrial superoxide production. Transgenic mice with human CAPN1 up-regulation restricted to mitochondria in cardiomyocytes (Tg-mtCapn1/tTA) were generated and characterized with low and high over-expression of transgenic human CAPN1 restricted to mitochondria, respectively...
March 15, 2019: Basic Research in Cardiology
Hye Kyoung Sung, Erfei Song, James Won Suk Jahng, Kostas Pantopoulos, Gary Sweeney
Iron overload is associated with various pathological changes which contribute to heart failure. Here, we examined mechanisms via which iron alters cardiomyocyte insulin sensitivity. Treatment of primary adult and neonatal cardiomyocytes as well as H9c2 cells with iron decreased insulin sensitivity determined via Western blotting or immunofluorescent detection of Akt and p70S6K phosphorylation and glucose uptake. Using CellROX deep red or DCF-DA probes we also observed that iron increased generation of reactive oxygen species (ROS), and that pretreatment with the superoxide dismutase mimetic MnTBAP reduced ROS production and attenuated iron-induced insulin resistance...
March 15, 2019: Scientific Reports
Azadeh Esfandiary, Hanna Kutsche, Rolf Schreckenberg, Martin Weber, Oleg Pak, Baktybek Kojonazarov, Akylbek Sydykov, Christine Hirschhäuser, Annemarie Wolf, Daniela Haag, Matthias Hecker, Ludger Fink, Werner Seeger, Hossein A Ghofrani, Ralph T Schermuly, Norbert Weißmann, Rainer Schulz, Susanne Rohrbach, Ling Li, Natascha Sommer, Klaus-Dieter Schlüter
AIMS: The role of uncoupling protein 2 (UCP2) in cardiac adaptation to pressure overload remains unclear. In a classical model of left ventricular pressure overload genetic deletion of UCP2 (UCP2-/-) protected against cardiac hypertrophy and failure. However, in UCP2-/- mice increased proliferation of pulmonary arterial smooth muscle cells induces mild pulmonary hypertension, right ventricular hypertrophy, and reduced cardiac output. This suggests a different role for UCP2 in right and left ventricular adaptation to pressure overload...
March 8, 2019: Cardiovascular Research
Qun Chen, Jeremy Thompson, Ying Hu, Anindita Das, Edward J Lesnefsky
Endoplasmic reticulum (ER) stress contributes to cardiovascular disease including heart failure. Interactions between the ER and mitochondria during ER stress can impair the mitochondrial respiratory chain and increase cell injury. p53 is a tumor suppressor protein that regulates apoptosis. p53 contributes to the regulation of mitochondrial and ER interactions, especially during the progression of ER stress. The knockout (KO) of p53 leads to decreased injury in hearts following ischemia-reperfusion. We asked if KO of p53 can protect mitochondria during the induction of ER stress and decrease cell injury...
2019: Frontiers in Cardiovascular Medicine
Jan Dudek, Magnus Hartmann, Peter Rehling
Mitochondria play an essential role in the energy metabolism of the heart. Many of the essential functions are associated with mitochondrial membranes and oxidative phosphorylation driven by the respiratory chain. Mitochondrial membranes are unique in the cell as they contain the phospholipid cardiolipin. The important role of cardiolipin in cardiovascular health is highlighted by several cardiac diseases, in which cardiolipin plays a fundamental role. Barth syndrome, Sengers syndrome, and Dilated cardiomyopathy with ataxia (DCMA) are genetic disorders, which affect cardiolipin biosynthesis...
April 1, 2019: Biochimica et biophysica acta. Molecular basis of disease
I M Studneva, M E Palkeeva, O M Veselova, A S Molokoedov, R O Lubimov, M V Ovchinnikov, M V Sidorova, O I Pisarenko
The use of the anticancer drug doxorubicin (Dox) is limited due to its cardiotoxic effect. Using the method of automatic solid-phase peptide synthesis, we obtained a synthetic agonist of galanin receptors GalR1-3 [RAla14, His15]-galanine (2-15) (G), exhibiting cardioprotective properties. It was purified by high performance liquid chromatography (HPLC). The homogeneity and structure of the peptide was confirmed by HPLC, 1H-NMR spectroscopy and mass spectroscopy. The purpose of this study was to study the effect of G on the metabolism and cardiac function of rats with chronic heart failure (CHF) caused by Dox...
January 2019: Biomedit︠s︡inskai︠a︡ Khimii︠a︡
Osamu Yamaguchi
The autophagic machinery is a well-conserved degradation system in eukaryotes from yeast to mammals. Autophagy has been thought of as a nonselective degradation process in which cytoplasmic proteins and organelles are degraded by fusion with lysosome. Recent studies have revealed selective forms of autophagy, such as mitochondria-specific autophagy, termed "mitophagy". Research over the past decade has revealed that autophagy in cardiomyocytes plays a protective role, not only during hemodynamic stress but in homeostasis during aging...
February 28, 2019: Circulation Journal: Official Journal of the Japanese Circulation Society
Daniela Sorriento, Jessica Gambardella, Antonella Fiordelisi, Guido Iaccarino, Maddalena Illario
Mitochondrial regulation of energy production, calcium homeostasis, and cell death are critical for cardiac function. Accordingly, the structural and functional abnormalities of these organelles (mitochondrial dysfunction) contribute to developing cardiovascular diseases and heart failure. Therefore the preservation of mitochondrial integrity is essential for cardiac cell survival. Mitochondrial function is regulated by several proteins, including GRK2 and β-arrestins which act in a GPCR independent manner to orchestrate intracellular signaling associated with key mitochondrial processes...
2019: Frontiers in Pharmacology
Nataliia V Shults, Sergey S Kanovka, Jennifer E Ten Eyck, Vladyslava Rybka, Yuichiro J Suzuki
Background Pulmonary arterial hypertension ( PAH ) is a serious disease without cure. Elevated pulmonary vascular resistance puts strain on the right ventricle ( RV ) and patients die of RV failure. Subjecting Sprague-Dawley rats to SU 5416 injection and hypoxia promotes severe PAH with pulmonary vascular lesions similar to human disease and has been well utilized to investigate pulmonary vascular pathology. However, despite exhibiting severe RV fibrosis, these rats do not die. Recently, subjecting Fischer ( CDF ) rats to the same treatment to promote PAH was found to result in mortality...
March 5, 2019: Journal of the American Heart Association
Melanie Ullrich, Benjamin Aßmus, Anne Marie Augustin, Hannes Häbich, Marco Abeßer, Jorge Martin Machado, Franziska Werner, Ralf Erkens, Anahi-Paula Arias-Loza, Sandra Umbenhauer, Helga Wagner, Peter M Benz, Andreas Unger, Wolfgang A Linke, Stefan Frantz, Hideo A Baba, Michaela Kuhn, Kai Schuh
Cardiac functionality is dependent on a balanced protein turnover. Accordingly, regulated protein decay is critical to maintain cardiac function. Here we demonstrate that deficiency of SPRED2, an intracellular repressor of ERK-MAPK signaling markedly expressed in human heart, resulted in impaired autophagy, heart failure, and shortened lifespan. SPRED2-/- mice showed cardiomyocyte hypertrophy, cardiac fibrosis, impaired electrical excitability, and severe arrhythmias. Mechanistically, cardiomyocyte dysfunction resulted from ERK hyperactivation and dysregulated autophagy, observed as accumulation of vesicles, vacuolar structures, and degenerated mitochondria...
February 13, 2019: Journal of Molecular and Cellular Cardiology
Jing Zhao, Jin-Lai Gao, Jun-Xue Zhu, Hai-Bin Zhu, Xuan Peng, Man Jiang, Yao Fu, Juan Xu, Xi-Hai Mao, Nan Hu, Ming-Hui Ma, De-Li Dong
Cardiomyocyte loss and cardiac fibrosis are the main characteristics of cardiac ischemia and heart failure, and mitochondrial function of cardiomyocytes is impaired in cardiac ischemia and heart failure, so the aim of this study is to identify fate variability of cardiomyocytes and cardiac fibroblasts with mitochondria inhibition and explore the underlying mechanism. The mitochondrial respiratory function was measured by using Oxygraph-2k high-resolution respirometry. The STAT3 expression and activity were evaluated by western blot...
February 14, 2019: Basic Research in Cardiology
Chowdhury S Abdullah, Shafiul Alam, Richa Aishwarya, Sumitra Miriyala, Mohammad Alfrad Nobel Bhuiyan, Manikandan Panchatcharam, Christopher B Pattillo, A Wayne Orr, Junichi Sadoshima, Joseph A Hill, Md Shenuarin Bhuiyan
Doxorubicin (Dox) is a highly effective anticancer drug but cause acute ventricular dysfunction, and also induce late-onset cardiomyopathy and heart failure. Despite extensive studies, the pathogenic sequelae leading to the progression of Dox-associated cardiomyopathy remains unknown. We assessed temporal changes in autophagy, mitochondrial dynamics, and bioenergetics in mouse models of acute and chronic Dox-cardiomyopathy. Time course study of acute Dox-treatment showed accumulation of LC3B II in heart lysates...
February 14, 2019: Scientific Reports
Yanhan Dong, Wenhua Xu, Cuiyun Liu, Peijun Liu, Peifeng Li, Kun Wang
Reactive oxygen species (ROS) are a class of reactive molecules that have been implicated in a variety of cardiovascular diseases, accompanied by disorder of multiple signaling events. As cardiomyocytes maintain abundant of mitochondria, which supply the major source of endogenous ROS, oxidative damage to mitochondria often drives apoptotic cell death and initiates cardiac pathology. In recent years, non-coding RNAs (ncRNAs) have received much attention to uncover their roles in regulating gene expression during those pathological events in the heart, such as myocardial infarction, cardiac hypertrophy, and heart failure...
2019: International Journal of Biological Sciences
Yuxiao Sun, Ying Cai, Qun S Zang
Sepsis is a leading cause of death in intensive care units, and cardiac dysfunction is an identified serious component of the multi-organ failure associated with this critical condition. This review summarized the current discoveries and hypothesizes of how autophagy changes in the heart during sepsis and the underlying mechanisms. Recent investigations suggest that specific activation of autophagy initiation factor Beclin-1 has a potential to protect cardiac mitochondria, attenuate inflammation, and improve cardiac function in sepsis...
February 10, 2019: Cells
Mark A Lampert, Amabel M Orogo, Rita H Najor, Babette C Hammerling, Leonardo J Leon, Bingyan J Wang, Taeyong Kim, Mark A Sussman, Åsa B Gustafsson
Cell-based therapies represent a very promising strategy to repair and regenerate the injured heart to prevent progression to heart failure. To date, these therapies have had limited success due to a lack of survival and retention of the infused cells. Therefore, it is important to increase our understanding of the biology of these cells and utilize this information to enhance their survival and function in the injured heart. Mitochondria are critical for progenitor cell function and survival. Here, we demonstrate the importance of mitochondrial autophagy, or mitophagy, in the differentiation process in adult cardiac progenitor cells (CPCs)...
February 11, 2019: Autophagy
Mariann Bombicz, Daniel Priksz, Rudolf Gesztelyi, Rita Kiss, Nora Hollos, Balazs Varga, Jozsef Nemeth, Attila Toth, Zoltan Papp, Zoltan Szilvassy, Bela Juhasz
Background and Aims : Diabetic cardiomyopathy (DCM) is an emerging problem worldwide due to an increase in the incidence of type 2 diabetes. Animal studies have indicated that metformin and pioglitazone can prevent DCM partly by normalizing insulin resistance, and partly by other, pleiotropic mechanisms. One clinical study has evidenced the insulin-senzitizing effect of the drug candidate BGP-15, along with additional animal studies that have confirmed its beneficial effects in models of diabetes, muscular dystrophy and heart failure, with the drug affecting chaperones, contractile proteins and mitochondria...
February 7, 2019: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
Xuexian Fang, Hao Wang, Dan Han, Enjun Xie, Xiang Yang, Jiayu Wei, Shanshan Gu, Feng Gao, Nali Zhu, Xiangju Yin, Qi Cheng, Pan Zhang, Wei Dai, Jinghai Chen, Fuquan Yang, Huang-Tian Yang, Andreas Linkermann, Wei Gu, Junxia Min, Fudi Wang
Heart disease is the leading cause of death worldwide. A key pathogenic factor in the development of lethal heart failure is loss of terminally differentiated cardiomyocytes. However, mechanisms of cardiomyocyte death remain unclear. Here, we discovered and demonstrated that ferroptosis, a programmed iron-dependent cell death, as a mechanism in murine models of doxorubicin (DOX)- and ischemia/reperfusion (I/R)-induced cardiomyopathy. In canonical apoptosis and/or necroptosis-defective Ripk3 -/- , Mlkl -/- , or Fadd -/- Mlkl -/- mice, DOX-treated cardiomyocytes showed features of typical ferroptotic cell death...
January 28, 2019: Proceedings of the National Academy of Sciences of the United States of America
Hani N Sabbah, Ramesh C Gupta, Vinita Singh-Gupta, Kefei Zhang
AIMS: Elamipretide (ELAM), an aromatic-cationic tetrapeptide, interacts with cardiolipin and normalizes dysfunctional mitochondria of cardiomyocytes. This study examined the effects of ELAM on skeletal muscle mitochondria function in dogs with chronic heart failure (HF). METHODS AND RESULTS: Studies were performed in skeletal muscle biopsy specimens obtained from normal dogs (n = 7) and dogs with chronic intracoronary microembolization-induced HF (n = 14) treated with subcutaneous ELAM 0...
January 28, 2019: ESC Heart Failure
Meghan C Hughes, Sofhia V Ramos, Patrick C Turnbull, Brittany A Edgett, Jason S Huber, Nazari Polidovitch, Uwe Schlattner, Peter H Backx, Jeremy A Simpson, Christopher G R Perry
KEY POINTS SUMMARY: -98% of patients with Duchenne muscular dystrophy (DMD) develop cardiomyopathy, with 40% developing heart failure -While increased propensity for mitochondrial induction of cell death has been observed in left ventricle, it remains unknown whether this is linked to impaired mitochondrial respiratory control and elevated H2 O2 emission prior to the onset of cardiomyopathy -Classic mouse models of DMD demonstrate hyper-regeneration in skeletal muscle which may mask mitochondrial abnormalities...
January 23, 2019: Journal of Physiology
Julie L Horton, Michael T Davidson, Clara Kurishima, Rick B Vega, Jeffery C Powers, Timothy R Matsuura, Christopher Petucci, E Douglas Lewandowski, Peter A Crawford, Deborah M Muoio, Fabio A Recchia, Daniel P Kelly
Evidence has emerged that the failing heart increases utilization of ketone bodies. We sought to determine whether this fuel shift is adaptive. Mice rendered incapable of oxidizing the ketone body 3-hydroxybutyrate (3OHB) in heart exhibited worsened heart failure in response to fasting or a pressure overload/ischemic insult compared to wild-type controls. Increased delivery of 3OHB ameliorated pathologic cardiac remodeling and dysfunction in mice and in a canine pacing model of progressive heart failure. 3OHB was shown to enhance bioenergetic thermodynamics of isolated mitochondria in the context of limiting levels of fatty acids...
January 22, 2019: JCI Insight
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