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Relevant bibliographies by topics / Heart – Hypertrophy

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Academic literature on the topic 'Heart – Hypertrophy'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 January 2023

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Journal articles on the topic "Heart – Hypertrophy"

1

Kang, Peter M., Patrick Yue, Zhilin Liu, Oleg Tarnavski, Natalya Bodyak, and Seigo Izumo. "Alterations in apoptosis regulatory factors during hypertrophy and heart failure." American Journal of Physiology-Heart and Circulatory Physiology 287, no. 1 (2004): H72—H80. http://dx.doi.org/10.1152/ajpheart.00556.2003.

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Cardiac hypertrophy from pathological stimuli often proceeds to heart failure, whereas cardiac hypertrophy from physiological stimuli does not. In this study, physiological hypertrophy was created by a daily exercise regimen and pathological hypertrophy was created from a high-salt diet in Dahl salt-sensitive rats. The rats continued on a high-salt diet progressed to heart failure associated with an increased rate of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. We analyzed primary cultures of these hearts and found that only cardiomyocytes made

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Liu, Yaoqiu, Yahui Shen, Jingai Zhu, et al. "Cardiac-Specific PID1 Overexpression Enhances Pressure Overload-Induced Cardiac Hypertrophy in Mice." Cellular Physiology and Biochemistry 35, no. 5 (2015): 1975–85. http://dx.doi.org/10.1159/000374005.

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Background/Aims: PID1 was originally described as an insulin sensitivity relevance protein, which is also highly expressed in heart tissue. However, its function in the heart is still to be elucidated. Thus this study aimed to investigate the role of PID1 in the heart in response to hypertrophic stimuli. Methods: Samples of human failing hearts from the left ventricles of dilated cardiomyopathy (DCM) patients undergoing heart transplants were collected. Transgenic mice with cardiomyocyte-specific overexpression of PID1 were generated, and cardiac hypertrophy was induced by transverse aortic co

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Kee, Hae Jin, and Hyun Kook. "Roles and Targets of Class I and IIa Histone Deacetylases in Cardiac Hypertrophy." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/928326.

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Cardiac hypertrophy occurs in association with heart diseases and ultimately results in cardiac dysfunction and heart failure. Histone deacetylases (HDACs) are post-translational modifying enzymes that can deacetylate histones and non-histone proteins. Research with HDAC inhibitors has provided evidence that the class I HDACs are pro-hypertrophic. Among the class I HDACs, HDAC2 is activated by hypertrophic stresses in association with the induction of heat shock protein 70. Activated HDAC2 triggers hypertrophy by inhibiting the signal cascades of either Krüppel like factor 4 (KLF4) or inositol

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Hu, Chengyun, Feibiao Dai, Jiawu Wang, et al. "Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice." Oxidative Medicine and Cellular Longevity 2022 (January 29, 2022): 1–12. http://dx.doi.org/10.1155/2022/5067544.

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A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown acceler

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Sarkar, Sagartirtha, Douglas W. Leaman, Sudhiranjan Gupta, et al. "Cardiac Overexpression of Myotrophin Triggers Myocardial Hypertrophy and Heart Failure in Transgenic Mice." Journal of Biological Chemistry 279, no. 19 (2004): 20422–34. http://dx.doi.org/10.1074/jbc.m308488200.

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Cardiac hypertrophy and heart failure remain leading causes of death in the United States. Many studies have suggested that, under stress, myocardium releases factors triggering protein synthesis and stimulating myocyte growth. We identified and cloned myotrophin, a 12-kDa protein from hypertrophied human and rat hearts. Myotrophin (whose gene is localized on human chromosome 7q33) stimulates myocyte growth and participates in cellular interaction that initiates cardiac hypertrophyin vitro. In this report, we present data on the pathophysiological significance of myotrophinin vivo, showing the

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Qian, Yanxia, Mingming Zhang, Ningtian Zhou, et al. "A long noncoding RNA CHAIR protects the heart from pathological stress." Clinical Science 134, no. 13 (2020): 1843–57. http://dx.doi.org/10.1042/cs20200149.

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Abstract Mammalian genomes have been found to be extensively transcribed. In addition to classic protein coding genes, a large numbers of long noncoding genes (lncRNAs) have been identified, while their functions, especially in heart diseases, remain to be established. We hypothesized that heart failure progression is controlled by tissue-specific lncRNAs. In the present study, we found that the cardiac-enriched lncRNA 4632428C04Rik, named as cardiomyocyte hypertrophic associated inhibitory RNA (CHAIR), is dynamically regulated during heart development, is expressed at low levels in embryonic

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Zhang, Yan, Qiang Da, Siyi Cao, et al. "HINT1 (Histidine Triad Nucleotide-Binding Protein 1) Attenuates Cardiac Hypertrophy Via Suppressing HOXA5 (Homeobox A5) Expression." Circulation 144, no. 8 (2021): 638–54. http://dx.doi.org/10.1161/circulationaha.120.051094.

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Background: Cardiac hypertrophy is an important prepathology of, and will ultimately lead to, heart failure. However, the mechanisms underlying pathological cardiac hypertrophy remain largely unknown. This study aims to elucidate the effects and mechanisms of HINT1 (histidine triad nucleotide–binding protein 1) in cardiac hypertrophy and heart failure. Methods: HINT1 was downregulated in human hypertrophic heart samples compared with nonhypertrophic samples by mass spectrometry analysis. Hint1 knockout mice were challenged with transverse aortic constriction surgery. Cardiac-specific overexpre

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SHANTZ, Lisa M., David J. FEITH та Anthony E. PEGG. "Targeted overexpression of ornithine decarboxylase enhances β-adrenergic agonist-induced cardiac hypertrophy". Biochemical Journal 358, № 1 (2001): 25–32. http://dx.doi.org/10.1042/bj3580025.

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These studies were designed to determine the consequences of constitutive overexpression of ornithine decarboxylase (ODC) in the heart. Induction of ODC is known to occur in response to agents that induce cardiac hypertrophy. However, it is not known whether high ODC levels are sufficient for the development of a hypertrophic phenotype. Transgenic mice were generated with cardiac-specific expression of a stable ODC protein using the α-myosin heavy-chain promoter. Founder lines with > 1000-fold overexpression of ODC in the heart were established, resulting in a 50-fold overaccumulation of pu

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Gu, Wei, Yutong Cheng, Su Wang, Tao Sun, and Zhizhong Li. "PHD Finger Protein 19 Promotes Cardiac Hypertrophy via Epigenetically Regulating SIRT2." Cardiovascular Toxicology 21, no. 6 (2021): 451–61. http://dx.doi.org/10.1007/s12012-021-09639-0.

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AbstractEpigenetic regulations essentially participate in the development of cardiomyocyte hypertrophy. PHD finger protein 19 (PHF19) is a polycomb protein that controls H3K36me3 and H3K27me3. However, the roles of PHF19 in cardiac hypertrophy remain unknown. Here in this work, we observed that PHF19 promoted cardiac hypertrophy via epigenetically targeting SIRT2. In angiotensin II (Ang II)-induced cardiomyocyte hypertrophy, adenovirus-mediated knockdown of Phf19 reduced the increase in cardiomyocyte size, repressed the expression of hypertrophic marker genes Anp and Bnp, as well as inhibited

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Funamoto, Masafumi, Yoichi Sunagawa, Yasufumi Katanasaka, et al. "Histone Acetylation Domains Are Differentially Induced during Development of Heart Failure in Dahl Salt-Sensitive Rats." International Journal of Molecular Sciences 22, no. 4 (2021): 1771. http://dx.doi.org/10.3390/ijms22041771.

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Histone acetylation by epigenetic regulators has been shown to activate the transcription of hypertrophic response genes, which subsequently leads to the development and progression of heart failure. However, nothing is known about the acetylation of the histone tail and globular domains in left ventricular hypertrophy or in heart failure. The acetylation of H3K9 on the promoter of the hypertrophic response gene was significantly increased in the left ventricular hypertrophy stage, whereas the acetylation of H3K122 did not increase in the left ventricular hypertrophy stage but did significantl

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Dissertations / Theses on the topic "Heart – Hypertrophy"

1

Paternostro, Giovanni. "Biochemical studies of cardiac hypertrophy." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337538.

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XU, JIAN. "TRANSCRIPTIONAL REGULATION OF CARDIAC HYPERTROPHY AND HEART FAILURE." University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1148396901.

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Drawnel, Faye Marie. "Control of myocardial hypertrophic remodelling by integration of calcium signals, kinase cascades and microRNAs." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609969.

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Archer, Caroline Rose. "Interactions between GPCR- and growth factor-activated signalling pathways in the induction of cardiac hypertrophy." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648427.

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Zhong, Tiecheng. "Ang II-Induced Cardiac Remodeling: Role of PI3-Kinase-Dependent Autophagy." Diss., North Dakota State University, 2018. https://hdl.handle.net/10365/28800.

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Heart failure (HF) is a pathological state indicating insufficient blood supply to the peripheral tissues from the heart. The pathophysiology of HF is multifactorial like cardiac remodeling including cardiac hypertrophy, perivascular fibrosis and apoptosis to compensate for the heart?s inability to pump enough blood. Cardiac hypertrophy is initially adaptive to hemodynamic overload; however, it chronically contributes to heart failure and sudden cardiac death. The extracellular regulatory factors and intracellular signaling pathways involved in the cardiac remodeling are not yet fully clear. P

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Müller-Brunotte, Richard. "Diastolic heart function in hypertension-induced left ventricular hypertrophy /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-898-3/.

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Turner, J. E. "Collagen metabolism in normal heart and during cardiac hypertrophy." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47290.

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Loonat, Aminah Ahmed. "The involvement of p38 gamma MAPK in pathological cardiac hypertrophy." Thesis, King's College London (University of London), 2016. http://kclpure.kcl.ac.uk/portal/en/theses/the-involvement-of-p38gamma-mapk-in-pathological-cardiac-hypertrophy(f00e26a7-dab2-474d-9d3e-a52dfe9e873e).html.

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p38-mitogen activated protein kinases (p38-MAPKs) are stress activated serine/threonine kinases that are activated during several different cardiac pathologies. Classically, studies have focused solely on p38α signaling in the heart. However, there is also high cardiac expression of the p38γ isoform but little is known about its cardiac function. The aim of this study was to elucidate the signaling pathway of p38γ, with a particular focus on its role in the progression of pathological cardiac hypertrophy. Comparisons of cardiac function and structure of wild type (WT) and p38γ knock out (KO) m

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Linehan, Katherine Alison. "Collagen deposition and myocyte hypertrophy in the pressure overloaded heart." Thesis, University of Hull, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484263.

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Benson, Victoria Louise St Vincent's Clinical School UNSW. "The role of calcineurin in high-renin and low-renin animal models of pressure overload left ventricular hypertrophy." Awarded by:University of New South Wales. St Vincent's Clinical School, 2005. http://handle.unsw.edu.au/1959.4/20843.

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Left ventricular hypertrophy (LVH) in response to pressure overload is associated with increased cardiovascular morbidity and mortality, making its prevention an important therapeutic goal. The role of a calcineurin-dependent molecular pathway in the induction of pressure-overload LVH is controversial. The present study tested the hypothesis that, in the setting of LV pressure overload, activation of the systemic renin-angiotensin system was necessary for activation of this calcineurin pathway. Mild LV pressure overload was induced in male Wistar rats by abdominal aortic constriction (AAC) or

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Books on the topic "Heart – Hypertrophy"

1

S, Dhalla Naranjan, and International Conference on Heart Failure (1994 : Winnipeg, Man.), eds. Heart hypertrophy and failure. Kluwer, 1995.

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2

Dhalla, Naranjan S., Grant N. Pierce, Vincenzo Panagia, and Robert E. Beamish, eds. Heart Hypertrophy and Failure. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4613-1237-6.

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3

Adami, J. George. Notes upon cardiac hypertrophy. s.n., 1985.

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Nobuakira, Takeda, Nagano Makoto 1928-, Dhalla Naranjan S, and International Conference on Cardiac Hypertrophy (1998 : Tokyo, Japan), eds. The hypertrophied heart. Kluwer Academic, 2000.

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5

Kirshenbaum, Lorrie A., Ian M. C. Dixon, and Pawan K. Singal, eds. Biochemistry of Hypertrophy and Heart Failure. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9238-3.

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6

Yang, Phillip Chung-Ming. Hypertrophic response in primary single-cell culture of adult rat myocardial cells. s.n.], 1989.

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7

A, Raineri, Leachman Robert D, and International School of Medical Sciences (1990 : Ettore Majorana Centre for Scientific Culture), eds. The big heart: Proceedings of a course held at the International School of Medical Sciences, Ettore Majorana Centre for Scientific Culture, Italy, 2-8 April 1990. Harwood Academic Publishers, 1994.

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8

Swynghedauw, B. Hypertrophie et insuffisance cardiaques. Editions INSERM, 1990.

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9

Verdecchia, Paolo. Management of left ventricular hypertrophy. Science Press, 2001.

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10

H, Messerli Franz, and Cruickshank J. M, eds. Left ventricular hypertrophy and its regression. Science Press, 1992.

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Book chapters on the topic "Heart – Hypertrophy"

1

Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, et al. "Heart Hypertrophy." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_878.

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2

Tio, R. A., R. de Boer, D. J. van Veldhuisen, and W. H. van Gilst. "The Role of Vascular Failure in Heart Failure." In Left Ventricular Hypertrophy. Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_2.

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Bontaş, Ecaterina, Florentina Radu-Ioniţă, and Liviu Stan. "Hypertrophy and Dilatation, Markers of Dysfunction." In Right Heart Pathology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73764-5_8.

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Pluim, B. M., A. van der Laarse, and E. E. van der Wall. "The Athlete’s Heart: A Physiological or a Pathological Phenomenon?" In Left Ventricular Hypertrophy. Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_7.

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Reichek, Nathaniel, and Martin G. St. John Sutton. "Left Ventricular Hypertrophy." In Two-Dimensional Real-Time Ultrasonic Imaging of the Heart. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2559-8_12.

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Chien, Kenneth R. "Molecular Physiology of Ventricular Hypertrophy." In Diastolic Relaxation of the Heart. Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2594-3_5.

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Marín-García, José. "Signaling in Hypertrophy and Heart Failure." In Signaling in the Heart. Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-9461-5_15.

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Lamb, H. J., A. de Roos, and E. E. van der Wall. "Left Ventricular Hypertrophic Heart Disease Studied by MR Imaging and 31P-MR Spectroscopy." In Left Ventricular Hypertrophy. Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_8.

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Zimmer, H. G. "Thyroid Hormones and Cardiac Hypertrophy." In Heart Function in Health and Disease. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-3090-9_18.

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Duncker, D. J. G. M. "Perfusion Abnormalities in the Hypertrophied Left Ventricle: Link Between Compensated Hypertrophy and Heart Failure?" In Left Ventricular Hypertrophy. Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4279-3_3.

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Conference papers on the topic "Heart – Hypertrophy"

1

Tretyn, Aleksandra, Soni Pullamsetti, Klaus-Dieter Schlueter, et al. "Wnt-Signaling Pathway In Experimental Right Heart Hypertrophy." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4982.

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García-Pelagio, Karla P., Ling Chen, and Robert J. Bloch. "Absence of synemin causes hypertrophy in murine heart." In MEDICAL PHYSICS: Fourteenth Mexican Symposium on Medical Physics. Author(s), 2016. http://dx.doi.org/10.1063/1.4954099.

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Farrar, G. E., and A. I. Veress. "A Coupled Model of LV Growth and Mechanics Applied to Pressure Overload Hypertrophy." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14557.

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Hypertension currently affects approximately one third the population in the United States, and represents a major economic burden on the health care system with an estimated annual direct and indirect cost of $50.6 billion [1]. In the case of systemic hypertension, the left ventricle (LV) must work against increased pressure load to pump blood to the body. Over time, this excessive work causes hypertrophy of the myocardium (thickening of the myofibers). While initially a compensatory mechanism, hypertrophy can eventually lead to heart failure (HF) [2]. Predictive modeling of the hypertrophic

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Xu Zhenyao and Fu Yinjie. "Application Of The Heart Model To Simulating Ventricle Hypertrophy." In Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.595856.

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Zhenyao, Xu, and Fu Yinjie. "Application of the heart model to simulating ventricle hypertrophy." In 1992 14th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 1992. http://dx.doi.org/10.1109/iembs.1992.5761242.

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Weixler, V., R. Lapusca, A. Guariento, et al. "Preventing Right Heart Failure in Pressure-Overload Hypertrophy through Transplantation of Autologous Mitochondria." In 48th Annual Meeting German Society for Thoracic, Cardiac, and Vascular Surgery. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678837.

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Makowiec, Danuta, Joanna Wdowczyk, and Marcin Gruchala. "Variability of heart rate variability indexes for estimates of left ventricular hypertrophy in subjects shortly after a heart transplant*." In 2022 12th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2022. http://dx.doi.org/10.1109/esgco55423.2022.9931353.

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Luitel, Himal, Akylbek Sydykov, Baktybek Kojonazarov, et al. "Contribution Of Progenitor Cells In Experimental Right Heart Hypertrophy Induced By Pulmonary Artery Ligation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4980.

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Lammers, Steven R., Phil H. Kao, Lian Tian, et al. "Quantification of Elastin Residual Stretch in Fresh Artery Tissue: Impact on Artery Material Properties and Pulmonary Hypertension Pathophysiology." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206793.

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Pulmonary arterial hypertension (PAH) is characterized as a chronic elevation in mean pulmonary artery pressure (MPAP) resulting from increased hydrodynamic resistance and decreased hydraulic capacitance of the pulmonary circulatory system. These hemodynamic changes cause the heart to operate outside optimum pump efficiency. The heart compensates for the efficiency loss through ventricular hypertrophy which, if left untreated, will continue until cardiac failure results.

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Wang, Lulu, and Ahmed Al-Jumaily. "A New GUI Device for Monitoring Cardiovascular Status." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-65361.

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Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Pulse wave velocity (PWV) is widely recognized as a significant marker of cardiovascular status monitoring, and it is correlated with many cardiovascular risk factors, including age, blood pressure, pulse pressure, hypertrophy and heart diseases. Aortic PWV is a direct measurement of aortic stiffness and is considered to be the gold standard of arterial stiffness measurements. This paper describes the development of a wireless healthcare device includes graphic user interface (GUI) to monitor the severity of CVD by measur

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Reports on the topic "Heart – Hypertrophy"

1

Cahaner, Avigdor, Sacit F. Bilgili, Orna Halevy, Roger J. Lien, and Kellye S. Joiner. effects of enhanced hypertrophy, reduced oxygen supply and heat load on breast meat yield and quality in broilers. United States Department of Agriculture, 2014. http://dx.doi.org/10.32747/2014.7699855.bard.

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Original objectivesThe objectives of this project were to evaluate the growth performance, meat yield and quality attributes of broiler strains widely differing in their genetic potential under normal temperature vs. warm temperature (short and long-term) conditions. Strain differences in breast muscle accretion rate, metabolic responses under heat load and, gross and histopathological changes in breast muscle under thermal load was also to be characterized. BackgroundTremendous genetic progress has been made in broiler chicken growth rate and meat yield since the 1950s. Higher growth rate is

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Yahav, Shlomo, John McMurtry, and Isaac Plavnik. Thermotolerance Acquisition in Broiler Chickens by Temperature Conditioning Early in Life. United States Department of Agriculture, 1998. http://dx.doi.org/10.32747/1998.7580676.bard.

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The research on thermotolerance acquisition in broiler chickens by temperature conditioning early in life was focused on the following objectives: a. To determine the optimal timing and temperature for inducing the thermotolerance, conditioning processes and to define its duration during the first week of life in the broiler chick. b. To investigate the response of skeletal muscle tissue and the gastrointestinal tract to thermal conditioning. This objective was added during the research, to understand the mechanisms related to compensatory growth. c. To evaluate the effect of early thermo cond

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Yahav, Shlomo, John Brake, and Orna Halevy. Pre-natal Epigenetic Adaptation to Improve Thermotolerance Acquisition and Performance of Fast-growing Meat-type Chickens. United States Department of Agriculture, 2009. http://dx.doi.org/10.32747/2009.7592120.bard.

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: The necessity to improve broiler thermotolerance and performance led to the following hypothesis: (a) thethermoregulatory-response threshold for heat production can be altered by thermal manipulation (TM) during incubation so as to improve the acquisition of thermotolerance in the post-hatch broiler;and (b) TM during embryogenesis will improve myoblast proliferation during the embryonic and post-hatch periods with subsequent enhanced muscle growth and meat production. The original objectives of this study were as follow: 1. to assess the timing, temperature, duration, and turning frequency r

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