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heart failure and autophagy

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https://www.readbyqxmd.com/read/28421194/dihydromyricetin-protects-against-diabetic-cardiomyopathy-in-streptozotocin-induced-diabetic-mice
#1
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
#2
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
#3
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
#4
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
#5
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
#6
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
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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...
February 24, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28216152/1-25-dihydroxyvitamin-d3-prevents-the-development-of-diabetic-cardiomyopathy-in-type-1-diabetic-rats-by-enhancing-autophagy-via-inhibiting-the-%C3%AE-catenin-tcf4-gsk-3%C3%AE-mtor-pathway
#15
Huili Wei, Hua Qu, Hang Wang, Baolan Ji, Yao Ding, Dan Liu, Yang Duan, Huimin Liang, Chuan Peng, Xiaoqiu Xiao, Huacong Deng
Diabetic cardiomyopathy (DCM) can increase the risk of heart failure and death in diabetic patients. However, no effective approaches are available to prevent its progression and development. Studies have shown that vitamin D is greatly implicated in cardiac hypertrophy and fibrosis, and there is a high prevalence of vitamin D deficiency in diabetic patients. In this study, we investigated whether 1,25-Dihydroxyvitamin-D3 (1,25D3) can improve DCM through a vitamin D receptor (VDR)-dependent mechanism associated with autophagy and the β-catenin/T-cell factor/lymphoid enhancer factor (TCF4)/glycogen synthase kinase-3β (GSK-3β)/mammalian target of rapamycin (mTOR) pathway...
April 2017: Journal of Steroid Biochemistry and Molecular Biology
https://www.readbyqxmd.com/read/28194437/mitochondrial-quality-control-dysregulation-in-conditional-ho-1-mice
#16
Hagir B Suliman, Jeffrey E Keenan, Claude A Piantadosi
The heme oxygenase-1 (Hmox1; HO-1) pathway was tested for defense of mitochondrial quality control in cardiomyocyte-specific Hmox1 KO mice (HO-1[CM](-/-)) exposed to oxidative stress (100% O2). After 48 hours of exposure, these mice showed persistent cardiac inflammation and oxidative tissue damage that caused sarcomeric disruption, cardiomyocyte death, left ventricular dysfunction, and cardiomyopathy, while control hearts showed minimal damage. After hyperoxia, HO-1(CM)(-/-) hearts showed suppression of the Pgc-1α/nuclear respiratory factor-1 (NRF-1) axis, swelling, low electron density mitochondria by electron microscopy (EM), increased cell death, and extensive collagen deposition...
February 9, 2017: JCI Insight
https://www.readbyqxmd.com/read/28166086/g%C3%AE-q-signaling-in-the-regulation-of-autophagy-and-heart-failure
#17
Mikhail A Kolpakov, Douglas G Tilley, Abdelkarim Sabri
No abstract text is available yet for this article.
April 2017: Journal of Cardiovascular Pharmacology
https://www.readbyqxmd.com/read/28164169/adeno-associated-virus-serotype-9-driven-expression-of-bag3-improves-left-ventricular-function-in-murine-hearts-with-left-ventricular-dysfunction-secondary-to-a-myocardial-infarction
#18
Tijana Knezevic, Valerie D Myers, Feifei Su, JuFang Wang, Jianliang Song, Xue-Qian Zhang, Erhe Gao, Guofeng Gao, Madesh Muniswamy, Manish K Gupta, Jennifer Gordon, Kristen N Weiner, Joseph Rabinowitz, Frederick V Ramsey, Douglas G Tilley, Kamel Khalili, Joseph Y Cheung, Arthur M Feldman
OBJECTIVES: The present study was undertaken to test the hypothesis that gene delivery of BCL2-Associated Athanogene 3 (BAG3) to the heart of mice with left ventricular dysfunction secondary to a myocardial infarction could enhance cardiac performance. BACKGROUND: BAG3 is a 575 amino acid protein that has pleotropic functions in the cell including pro-autophagy and anti-apoptosis. Mutations in BAG3 have been associated with both skeletal muscle dysfunction and familial dilated cardiomyopathy and BAG3 levels are diminished in non-familial heart failure...
December 2016: JACC. Basic to Translational Science
https://www.readbyqxmd.com/read/28151473/knockout-of-eva1a-leads-to-rapid-development-of-heart-failure-by-impairing-autophagy
#19
Shu Zhang, Xin Lin, Ge Li, Xue Shen, Di Niu, Guang Lu, Xin Fu, Yingyu Chen, Ming Cui, Yun Bai
EVA1A (Eva-1 homologue A) is a novel lysosome and endoplasmic reticulum-associated protein that can regulate cell autophagy and apoptosis. Eva1a is expressed in the myocardium, but its function in myocytes has not yet been investigated. Therefore, we generated inducible, cardiomyocyte-specific Eva1a knockout mice with an aim to determine the role of Eva1a in cardiac remodelling in the adult heart. Data from experiments showed that loss of Eva1a in the adult heart increased cardiac fibrosis, promoted cardiac hypertrophy, and led to cardiomyopathy and death...
February 2, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28130111/microrna-365-accelerates-cardiac-hypertrophy-by-inhibiting-autophagy-via-the-modulation-of-skp2-expression
#20
Haibo Wu, Yuncan Wang, Xuechao Wang, Ruyi Li, Deyun Yin
Evidence is emerging of a tight link between cardiomyocyte autophagy and cardiac hypertrophy (CH). Sustained exposure to stress leads CH to progress to heart failure. Several miRNAs have been described in heart failure, and miRNA-based therapeutic approaches are being pursued. Although microRNA-365 (miR-365) has been testified as a positive modulator of CH, the specific mechanism remains unclear. In the present study, we observed that miR-365 expression was up-regulated in hypertrophic cardiomyocytes both in vivo and in vitro, and was accompanied by dysregulation of autophagy...
January 24, 2017: Biochemical and Biophysical Research Communications
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