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heart failure and autophagy

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https://www.readbyqxmd.com/read/28526246/impaired-mitophagy-facilitates-mitochondrial-damage-in-danon-disease
#1
Sherin I Hashem, Anne N Murphy, Ajit S Divakaruni, Matthew L Klos, Bradley C Nelson, Emily C Gault, Teisha J Rowland, Cynthia N Perry, Yusu Gu, Nancy D Dalton, William H Bradford, Eric J Devaney, Kirk L Peterson, Kenneth L Jones, Matthew R G Taylor, Ju Chen, Neil C Chi, Eric D Adler
RATIONALE: Lysosomal associated membrane protein type-2 (LAMP-2) is a highly conserved, ubiquitous protein that is critical for autophagic flux. Loss of function mutations in the LAMP-2 gene cause Danon disease, a rare X-linked disorder characterized by developmental delay, skeletal muscle weakness, and severe cardiomyopathy. We previously found that human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) from Danon patients exhibited significant mitochondrial oxidative stress and apoptosis...
May 16, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28515362/insulin-supplementation-attenuates-cancer-induced-cardiomyopathy-and-slows-tumor-disease-progression
#2
James T Thackeray, Stefan Pietzsch, Britta Stapel, Melanie Ricke-Hoch, Chun-Wei Lee, Jens P Bankstahl, Michaela Scherr, Jörg Heineke, Gesine Scharf, Arash Haghikia, Frank M Bengel, Denise Hilfiker-Kleiner
Advanced cancer induces fundamental changes in metabolism and promotes cardiac atrophy and heart failure. We discovered systemic insulin deficiency in cachectic cancer patients. Similarly, mice with advanced B16F10 melanoma (B16F10-TM) or colon 26 carcinoma (C26-TM) displayed decreased systemic insulin associated with marked cardiac atrophy, metabolic impairment, and function. B16F10 and C26 tumors decrease systemic insulin via high glucose consumption, lowering pancreatic insulin production and producing insulin-degrading enzyme...
May 18, 2017: JCI Insight
https://www.readbyqxmd.com/read/28494450/stachydrine-protects-against-pressure-overload-induced-cardiac-hypertrophy-by-suppressing-autophagy
#3
Tong-Tong Cao, Hui-Hua Chen, Zhiwei Dong, Yan-Wu Xu, Pei Zhao, Wei Guo, Hong-Chang Wei, Chen Zhang, Rong Lu
BACKGROUND: Autophagy is required for the maintenance of cardiomyocyte homeostasis. However, excessive autophagy plays a maladaptive role in pressure overload-induced heart failure. To identify mechanisms by which Stachydrine inhibits pressure overload-induced cardiac hypertrophy, we determined inhibitory activities against activation of NADPH oxidase, reactive oxygen species(ROS) production and excessive activation of autophagy. METHODS: Stachydrine was administered intragastrically to Wistar rats after Transverse aortic constriction(TAC) and H9c2 cells were treated with Stachydrine after Angiotension II stimulation...
May 11, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28493471/what-role-does-the-stress-response-have-in-congestive-heart-failure
#4
REVIEW
Ahmed Badreddin, Youssef Fady, Hamdy Attia, Mohamed Hafez, Ahmed Khairallah, Dina Johar, Larry Bernstein
This review is concerned with cardiac malfunction as a result of an imbalance in protein proteostasis, the homeostatic balance between protein removal and regeneration in a long remodeling process involving the endoplasmic reticulum (ER) and the unfolded protein response (UPR). The importance of this is of special significance with regard to cardiac function as a high energy requiring muscular organ that has a high oxygen requirement and is highly dependent on mitochondria. The importance of mitochondria is not only concerned with high energy dependence on mitochondrial electron transport, but it also has a role in the signaling between the mitochondria and the ER under stress...
May 11, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28487390/activation-of-the-amino-acid-response-pathway-blunts-the-effects-of-cardiac-stress
#5
Pu Qin, Pelin Arabacilar, Roberta E Bernard, Weike Bao, Alan R Olzinski, Yuanjun Guo, Hind Lal, Stephen H Eisennagel, Michael C Platchek, Wensheng Xie, Julius Del Rosario, Mohamad Nayal, Quinn Lu, Theresa Roethke, Christine G Schnackenberg, Fe Wright, Michael P Quaile, Wendy S Halsey, Ashley M Hughes, Ganesh M Sathe, George P Livi, Robert B Kirkpatrick, Xiaoyan A Qu, Deepak K Rajpal, Maria Faelth Savitski, Marcus Bantscheff, Gerard Joberty, Giovanna Bergamini, Thomas L Force, Gregory J Gatto, Erding Hu, Robert N Willette
BACKGROUND: The amino acid response (AAR) is an evolutionarily conserved protective mechanism activated by amino acid deficiency through a key kinase, general control nonderepressible 2. In addition to mobilizing amino acids, the AAR broadly affects gene and protein expression in a variety of pathways and elicits antifibrotic, autophagic, and anti-inflammatory activities. However, little is known regarding its role in cardiac stress. Our aim was to investigate the effects of halofuginone, a prolyl-tRNA synthetase inhibitor, on the AAR pathway in cardiac fibroblasts, cardiomyocytes, and in mouse models of cardiac stress and failure...
May 9, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28455287/desmin-loss-and-mitochondrial-damage-precede-left-ventricular-systolic-failure-in-volume-overload-heart-failure
#6
Jason Guichard, Michael Paul Rogowski, Giulio Agnetti, Lianwu Fu, Pamela Powell, Chih-Chang Wei, James F Collawn, Louis J Dell'Italia
BACKGROUND: Heart failure due to chronic volume overload (VO) in the rat and human is characterized by disorganization of cardiomyocyte desmin/mitochondrial network. Here we test the hypothesis that desmin breakdown is an early and continuous process throughout VO. METHODS: Male Sprague-Dawley rats had aortocaval fistula (ACF) or sham surgery for 24 hours, 4 weeks or 12 weeks (wk). Desmin/mitochondrial ultrastructure was examined by transmission electron microscopy (TEM) and immunohistochemistry (IHC)...
April 28, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28421194/dihydromyricetin-protects-against-diabetic-cardiomyopathy-in-streptozotocin-induced-diabetic-mice
#7
Bin Wu, Jie Lin, Jian Luo, Dong Han, Miaomiao Fan, Tao Guo, Ling Tao, Ming Yuan, Fu Yi
Diabetic cardiomyopathy (DCM) is an important cause of heart failure in diabetic patients. The present study sought to explore the potential effects of dihydromyricetin (DHM) on DCM and its possible mechanism. A diabetic model was induced by intraperitoneal injection of streptozotocin (STZ) in C57BL/6J mice. Two weeks after the STZ injection, mice were randomly allocated into the following 4 groups for treatment: the control group (CON), the control treated with DHM group (CON + DHM), the diabetes group (DM), and the diabetes treated with DHM group (DM + DHM)...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28390176/cucurbitacin-b-protects-against-pressure-overload-induced-cardiac-hypertrophy
#8
Yang Xiao, Zheng Yang, Qing-Qing Wu, Xiao-Han Jiang, Yuan Yuan, Wei Chang, Zhou Yan Bian, Jin Xiu Zhu, Qi-Zhu Tang
Lack of effective anti-cardiac hypertrophy drugs creates a major cause for the increasing prevalence of heart failure. In the present study, we determined the anti-hypertrophy and anti-fibrosis potential of a natural plant triterpenoid, Cucurbitacin B both in vitro and in vivo. Aortic banding (AB) was performed to induce cardiac hypertrophy. After 1 week of surgery, mice were receive cucurbitacin B treatment (Gavage, 0.2 mg/kg body weight/2 day). Afer 4 weeks of AB, cucurbitacin B demonstrated a strong anti- hypertrophy and anti-fibrosis ability as evidenced by decreased of heart weight, myocardial cell cross-sectional area and interstitial fibrosis, ameliorated of systolic and diastolic abnormalities, normalized in gene expression of hypertrophic and fibrotic markers, reserved microvascular density in pressure overload induced hypertrophic mice...
April 8, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28389131/autophagy-metabolic-disease-and-pathogenesis-of-heart-dysfunction
#9
REVIEW
Fulong Wang, Jocelyn Jia, Brian Rodrigues
In normal physiology, autophagy is recognized as a protective housekeeping mechanism that enables elimination of unhealthy organelles, protein aggregates, and invading pathogens, as well as recycling cell components and producing new building blocks and energy for cellular renovation and homeostasis. However, overactive or depressed autophagy is often associated with the pathogenesis of multiple disorders, including cardiac disease. During metabolic disorders, such as diabetes and obesity, dysregulation of autophagy frequently leads to cell death, cardiomyopathy, and cardiac dysfunction...
January 14, 2017: Canadian Journal of Cardiology
https://www.readbyqxmd.com/read/28381696/sterile-inflammation-and-degradation-systems-in-heart-failure
#10
Kazuhiko Nishida, Kinya Otsu
In most patients with chronic heart failure (HF), levels of circulating cytokines are elevated and the elevated cytokine levels correlate with the severity of HF and prognosis. Various stresses induce subcellular component abnormalities, such as mitochondrial damage. Damaged mitochondria induce accumulation of reactive oxygen species and apoptogenic proteins, and subcellular inflammation. The vicious cycle of subcellular component abnormalities, inflammatory cell infiltration and neurohumoral activation induces cardiomyocyte injury and death, and cardiac fibrosis, resulting in cardiac dysfunction and HF...
April 5, 2017: Circulation Journal: Official Journal of the Japanese Circulation Society
https://www.readbyqxmd.com/read/28376509/activation-of-g%C3%AE-q-in-cardiomyocytes-increases-vps34-activity-and-stimulates-autophagy
#11
Shengnan Liu, Ya-Ping Jiang, Lisa M Ballou, Wei-Xing Zong, Richard Z Lin
Receptors that activate the heterotrimeric G protein Gαq are thought to play a role in the development of heart failure. Dysregulation of autophagy occurs in some pathological cardiac conditions including heart failure, but whether Gαq is involved in this process is unknown. We used a cardiomyocyte-specific transgenic mouse model of inducible Gαq activation (termed GαqQ209L) to address this question. After 7 days of Gαq activation, GαqQ209L hearts contained more autophagic vacuoles than wild type hearts...
April 2017: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28362341/the-role-of-micrornas-in-myocardial-infarction-from-molecular-mechanism-to-clinical-application
#12
REVIEW
Teng Sun, Yan-Han Dong, Wei Du, Chun-Ying Shi, Kun Wang, Muhammad-Akram Tariq, Jian-Xun Wang, Pei-Feng Li
MicroRNAs (miRNAs) are a class of small single-stranded and highly conserved non-coding RNAs, which are closely linked to cardiac disorders such as myocardial infarction (MI), cardiomyocyte hypertrophy, and heart failure. A growing number of studies have demonstrated that miRNAs determine the fate of the heart by regulating cardiac cell death and regeneration after MI. A deep understanding of the pathophysiology of miRNA dependent regulatory pathways in these processes is required. The role of miRNAs as diagnostic, prognostic, and therapeutic targets also needs to be explored in order to utilize them in clinical settings...
March 31, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28361977/myocardial-stress-and-autophagy-mechanisms-and-potential-therapies
#13
REVIEW
Lea M D Delbridge, Kimberley M Mellor, David J Taylor, Roberta A Gottlieb
Autophagy is a ubiquitous cellular catabolic process responsive to energy stress. Research over the past decade has revealed that cardiomyocyte autophagy is a prominent homeostatic pathway, important in adaptation to altered myocardial metabolic demand. The cellular machinery of autophagy involves targeted direction of macromolecules and organelles for lysosomal degradation. Activation of autophagy has been identified as cardioprotective in some settings (that is, ischaemia and ischaemic preconditioning). In other situations, sustained autophagy has been linked with cardiopathology (for example, sustained pressure overload and heart failure)...
March 31, 2017: Nature Reviews. Cardiology
https://www.readbyqxmd.com/read/28347844/complex-inhibition-of-autophagy-by-mitochondrial-aldehyde-dehydrogenase-shortens-lifespan-and-exacerbates-cardiac-aging
#14
Yingmei Zhang, Cong Wang, Jingmin Zou, Aijun Sun, Lindsay K Hueckstaedt, Junbo Ge, Jun Ren
Autophagy, a conservative degradation process for long-lived and damaged proteins, participates in a cascade of biological processes including aging. A number of autophagy regulators have been identified. Here we demonstrated that mitochondrial aldehyde dehydrogenase (ALDH2), an enzyme with the most common single point mutation in humans, governs cardiac aging through regulation of autophagy. Myocardial mechanical and autophagy properties were examined in young (4 mo) and old (26-28 mo) wild-type (WT) and global ALDH2 transgenic mice...
March 24, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28342806/molecular-regulation-of-mitochondrial-dynamics-in-cardiac-disease
#15
REVIEW
Jinliang Nan, Wei Zhu, M S Rahman, Mingfei Liu, Dan Li, Shengan Su, Na Zhang, Xinyang Hu, Hong Yu, Mahesh P Gupta, Jian'an Wang
Mitochondrial homeostasis is critical for keeping functional heart in response to metabolic or environmental stresses. Mitochondrial fission and fusion (mitochondrial dynamics) play essential roles in maintaining mitochondrial homeostasis, defects in mitochondrial dynamics lead to cardiac diseases such as ischemia-reperfusion injury (IRI), heart failure and diabetic cardiomyopathy. Mitochondrial dynamics is determined by mitochondrial fission and fusion proteins, including OPA1, mitofusins and Drp1. These proteins are tightly regulated by a series of signaling pathways through different aspects such as transcription, post translation modifications (PTMs) and proteasome-dependent protein degradation...
March 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28336438/klf15-protects-against-isoproterenol-induced-cardiac-hypertrophy-via-regulation-of-cell-death-and-inhibition-of-akt-mtor-signaling
#16
Li Gao, Yudong Guo, Xiaofeng Liu, Deya Shang, Yongjian Du
Increasing evidence indicate that the Krüppel-like factor KLF15, a member of Cys2/His2 zinc-finger DNA-binding proteins, attenuates cardiac hypertrophy. However, the role of KLF15 in cardiovascular system is largely unknown and the exact molecular mechanism of its protective function is not fully elucidated. In the present study, we established a mouse model of cardiac hypertrophy and found that KLF15 expression was down-regulated in hypertrophic hearts. To evaluate the roles of KLF15 in cardiac hypertrophy, we generated transgenic mice overexpressing KLF15 of KLF15 knockdown mice and subsequently induced cardiac hypertrophy...
May 20, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28300155/volume-sensitive-outwardly-rectifying-chloride-channel-blockers-protect-against-high-glucose-induced-apoptosis-of-cardiomyocytes-via-autophagy-activation
#17
Lin Wang, Mingzhi Shen, Xiaowang Guo, Bo Wang, Yuesheng Xia, Ning Wang, Qian Zhang, Lintao Jia, Xiaoming Wang
Hyperglycemia is a well-characterized contributing factor for cardiac dysfunction and heart failure among diabetic patients. Apoptosis of cardiomyocytes plays a major role during the onset and pathogenesis of diabetic cardiomyopathy (DCM). Nonetheless, the molecular machinery underlying hyperglycemia-induced cardiac damage and cell death remains elusive. In the present study, we found that chloride channel blockers, 4,4'-diisothiocya-natostilbene-2,2'- disulfonic acid (DIDS) and 4-(2-butyl-6,7-dichlor-2-cyclopentyl-indan-1-on-5-yl) oxybutyric acid (DCPIB), inhibited high glucose-activated volume-sensitive outwardly rectifying (VSOR) Cl(-) channel and improved the viability of cardiomyocytes...
March 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28246204/science-signaling-podcast-for-28-february-2017-balancing-autophagy-in-the-stressed-heart
#18
Saumya Das, Annalisa M VanHook
This Podcast features an interview with Saumya Das, senior author of a Research Article that appears in the 28 February 2017 issue of Science Signaling, about a protein that inhibits pathological cardiac hypertrophy in mice. Temporary increases in cardiac workload, such as those caused by exercise or pregnancy, induce physiological cardiac hypertrophy, a beneficial type of heart enlargement that is adaptive. However, a sustained increase in workload due to metabolic stress or uncontrolled high blood pressure induces pathological cardiac hypertrophy, which can contribute to heart failure...
February 28, 2017: Science Signaling
https://www.readbyqxmd.com/read/28246202/ddit4l-promotes-autophagy-and-inhibits-pathological-cardiac-hypertrophy-in-response-to-stress
#19
Bridget Simonson, Vinita Subramanya, Mun Chun Chan, Aifeng Zhang, Hannabeth Franchino, Filomena Ottaviano, Manoj K Mishra, Ashley C Knight, Danielle Hunt, Ionita Ghiran, Tejvir S Khurana, Maria I Kontaridis, Anthony Rosenzweig, Saumya Das
Physiological cardiac hypertrophy, in response to stimuli such as exercise, is considered adaptive and beneficial. In contrast, pathological cardiac hypertrophy that arises in response to pathological stimuli such as unrestrained high blood pressure and oxidative or metabolic stress is maladaptive and may precede heart failure. We found that the transcript encoding DNA damage-inducible transcript 4-like (DDiT4L) was expressed in murine models of pathological cardiac hypertrophy but not in those of physiological cardiac hypertrophy...
February 28, 2017: Science Signaling
https://www.readbyqxmd.com/read/28238768/regulation-of-autophagy-by-some-natural-products-as-a-potential-therapeutic-strategy-for-cardiovascular-disorders
#20
REVIEW
Mahmoud Hashemzaei, Reza Entezari Heravi, Ramin Rezaee, Ali Roohbakhsh, Gholamreza Karimi
Autophagy is a lysosomal degradation process through which long-lived and misfolded proteins and organelles are sequestered, degraded by lysosomes, and recycled. Autophagy is an essential part of cardiomyocyte homeostasis and increases the survival of cells following cellular stress and starvation. Recent studies made clear that dysregulation of autophagy in the cardiovascular system leads to heart hypertrophy and failure. In this manner, autophagy seems to be an attractive target in the new treatment of cardiovascular diseases...
May 5, 2017: European Journal of Pharmacology
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