- abnormal enlargement of a body part or organ
- undergo hypertrophy; "muscles can hypertrophy when people take steroids"
- increase in size, magnitude, number, or intensity; "The music swelled to a crescendo"
- expand abnormally; "The bellies of the starving children are swelling" (同)swell up, intumesce, tumefy, tumesce
- cause to become swollen; "The water swells the wood"
- a crescendo followed by a decrescendo
- the undulating movement of the surface of the open sea (同)crestless wave
- a rounded elevation (especially one on an ocean floor)
- become filled with pride, arrogance, or anger; "The mother was swelling with importance when she spoke of her son" (同)puff_up
- make viscous or dense; "thicken the sauce by adding flour" (同)inspissate
- become thick or thicker; "The sauce thickened"; "The egg yolk will inspissate" (同)inspissate
- make thick or thicker; "Thicken the sauce"; "inspissate the tar so that it becomes pitch" (同)inspissate
- becoming more intricate or complex; "a thickening plot"
- any material used to thicken; "starch is used in cooking as a thickening" (同)thickener
- the act of thickening (同)inspissation
- 〈物が〉『大きくなる』,ふくれる,はれる《+up》 / 〈帆などが〉『張り出る』,ふくらむ《+out》 / 〈数量・程度・力などが〉『増大する』,増える,強まる / 〈川などが〉増水する,〈海が〉うねる,〈土地が〉高まる / 《話》〈感情が〉高まる;(感情で)〈胸が〉いっぱいになる《+with+名》 / …‘を'『ふくらます』,‘の'かさを大きくする / 〈帆など〉‘を'『張り出させる』,ふくらませる《+out+名,+名+out》 / …‘を'『増大させる』,増やす,強める / 〈心・胸など〉‘を'いっぱいにする / 〈U〉《時にa ~》ふくれる(増大する)こと;ふくれている状態 / 〈C〉土地の隆起部,なだらかな丘 / 〈U〉《単数形で》大波,うねり / 〈C〉音の高まり,音量の増減 / 〈C〉《古》《話》名士;(特に)流行の服を着た人 / 《米話》すばらしい,すてきな / 《古》《俗》いきな,しゃれた
- …‘を'厚くする;…‘を'濃くする / 厚くなる;濃くなる / 〈話の筋などが〉複雑になる
- 厚くする(なる)こと / 厚くなった部分 / 濃縮材料
||This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (September 2014)
Hypertrophy results from an increase in cell size, whereas hyperplasia stems from an increase in cell number
|Classification and external resources
|-plasia and -trophy
- Anaplasia (structural differentiation loss within cell or group of cells)
- Aplasia (organ or part of organ missing)
- Hypoplasia (congenital below-average number of cells, especially when inadequate)
- Hyperplasia (proliferation of cells)
- Neoplasia (abnormal proliferation)
- Dysplasia (change in cell or tissue phenotype)
- Metaplasia (conversion in cell type)
- Prosoplasia (development of new cell function)
- Desmoplasia (connective tissue growth)
- Atrophy (reduced functionality of an organ, with decrease in the number or volume of cells)
- Hypertrophy (increase in the volume of cells)
Forensic post-mortem examination of a case of hypertrophic cardiomyopathy, showing thickening of the cardiac muscle.
Hypertrophy (from Greek ὑπέρ "excess" + τροφή "nourishment") is the increase in the volume of an organ or tissue due to the enlargement of its component cells. It is distinguished from hyperplasia, in which the cells remain approximately the same size but increase in number. Although hypertrophy and hyperplasia are two distinct processes, they frequently occur together, such as in the case of the hormonally-induced proliferation and enlargement of the cells of the uterus during pregnancy.
Eccentric hypertrophy is a type of hypertrophy where the walls and chamber of a hollow organ undergo growth in which the overall size and volume are enlarged. It is applied especially to the left ventricle of heart. Sarcomeres are added in series, as for example in dilated cardiomyopathy (in contrast to hypertrophic cardiomyopathy, a type of concentric hypertrophy, where sarcomeres are added in parallel).
- Athlete's heart
- Ventricular hypertrophy (including left ventricular hypertrophy and right ventricular hypertrophy)
- ^ Kusumoto, F. M. (2004), Cardiovascular Pathophysiology, Hayes Barton Press, pp. 20–22, ISBN 978-1-59377-189-8
- University of California Muscle Physiology Home Page: Hypertrophy
|Principles of pathology
- Cell damage
- Wound healing
- Cellular adaptation
- Cell death
- Liquefactive necrosis
- Coagulative necrosis
- Caseous necrosis
- Fat necrosis
- Programmed cell death
- Surgical pathology
- Molecular pathology
- Forensic pathology
- Oral and maxillofacial pathology
- Gross examination
- Electron microscopy
- Fluorescence in situ hybridization
- Clinical chemistry
- Transfusion medicine
- Medical microbiology
- Diagnostic immunology
- Enzyme assay
- Mass spectrometry
- Flow cytometry
- Blood bank
- Microbiological culture
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- Efficacy and safety of incobotulinum toxin A in periocular rhytides and masseteric hypertrophy: side-by-side comparison with onabotulinum toxin A.
- Lee JH, Park JH, Lee SK, Han KH, Kim SD, Yoon CS, Park JY, Lee JH, Yang JM, Lee JH.Author information Department of Dermatology, Samsung Medical Center, Sungkyunkwan University School of Medicine , Seoul , Republic of Korea.AbstractBACKGROUND: Incobotulinum is a newly developed botulinum toxin A in which the complexing proteins had been removed.
- The Journal of dermatological treatment.J Dermatolog Treat.2014 Aug;25(4):326-30. doi: 10.3109/09546634.2013.769041. Epub 2013 Jun 2.
- BACKGROUND: Incobotulinum is a newly developed botulinum toxin A in which the complexing proteins had been removed.OBJECTIVE: The aim was to compare the efficacy and safety of incobotulinum with onabotulinum in treating periocular rhytides and masseteric hypertrophy.METHODS: A randomized, double-bli
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- The Many Lives of CTIP2: From AIDS to Cancer and Cardiac Hypertrophy.
- Le Douce V, Cherrier T, Riclet R, Rohr O, Schwartz C.Author information Institut de Parasitologie et de Pathologie Tropicale, EA7292, Université de Strasbourg, Strasbourg, France; IUT de Schiltigheim, 1 Allée d'Athènes, Schiltigheim, France.AbstractCTIP2 is a key transcriptional regulator involved in numerous physiological functions. Initial works have shown the importance of CTIP2 in the establishment and persistence of HIV latency in microglial cells, the main latent/quiescent viral reservoir in the brain. Recent studies have highlighted the importance of CTIP2 in several other pathologies, such as cardiac hypertrophy and various types of human malignancies. Targeting CTIP2 may therefore constitute a new approach in the treatment of these pathologies. J. Cell. Physiol. 229: 533-537, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular physiology.J Cell Physiol.2014 May;229(5):533-7. doi: 10.1002/jcp.24490.
- CTIP2 is a key transcriptional regulator involved in numerous physiological functions. Initial works have shown the importance of CTIP2 in the establishment and persistence of HIV latency in microglial cells, the main latent/quiescent viral reservoir in the brain. Recent studies have highlighted the
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- Angiotensin II and the ERK pathway mediate the induction of leptin by mechanical cyclic stretch in cultured rat neonatal cardiomyocytes.
- Chiu CZ, Wang BW, Shyu KG.AbstractMechanical cyclic stretch of cardiomyocytes causes cardiac hypertrophy through cardiac-restricted gene expression. Leptin induces cardiomyocyte hypertrophy in response to myocardial stress. In the present study, we evaluated the expression of leptin under cyclic stretch and its role in regulating genetic transcription in cardiomyocytes. Cultured rat neonatal cardiomyocytes were subjected to cyclic stretch, and the expression levels of leptin, ROS (reactive oxygen species) and AngII (angiotensin II) were evaluated. Signal transduction inhibitors were used to identify the pathway of leptin expression. EMSAs were used to identify the binding of leptin/STAT3 (signal transducer and activator of transcription 3) and luciferase assays were used to identify the transcription of leptin in cardiomyocytes. The study also used an in vivo model of AV (aortocaval) shunt in rats to investigate leptin, ROS and AngII expression. Leptin and leptin receptor levels increased after cyclic stretch with the earlier expression of AngII and ROS. Leptin expression was suppressed by AngII receptor blockers, an ROS scavenger [NAC (N-acetylcysteine)], an ERK (extracellular-signal-regulated kinase) pathway inhibitor (PD98059) and ERK siRNA. Binding of leptin/STAT3 was identified by EMSAs, and luciferase assays confirmed the transcription of leptin in neonatal cardiomyocytes after cyclic stretch. Increased MHC (myosin heavy chain) expression and [3H]-proline incorporation in cardiomyocytes was detected after cyclic stretch, which were inhibited by leptin siRNA and NAC. The in vivo model of AV shunt also demonstrated increased levels of plasma and myocardial leptin, ROS and AngII expression after cyclic stretch. Mechanical cyclic stretch in cardiomyocytes increased leptin expression mediated by the induction of AngII, ROS and the ERK pathway to cause cardiomyocyte hypertrophy. Myocardial hypertrophy can be identified by increased transcriptional activity and an enhanced hypertrophic phenotype of cardiomyocytes.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Apr;126(7):483-95. doi: 10.1042/CS20130235.
- Mechanical cyclic stretch of cardiomyocytes causes cardiac hypertrophy through cardiac-restricted gene expression. Leptin induces cardiomyocyte hypertrophy in response to myocardial stress. In the present study, we evaluated the expression of leptin under cyclic stretch and its role in regulating ge
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- Role of Heterotrimeric G Protein and Calcium in Cardiomyocyte Hypertrophy Induced by IGF-1.
- Carrasco L, Cea P, Rocco P, Peña-Oyarzún D, Rivera-Mejias P, Sotomayor-Flores C, Quiroga C, Criollo A, Ibarra C, Chiong M, Lavandero S.Author information Advanced Center for Chronic Diseases, Universidad de Chile, Santiago, Chile; Centro Estudios Moleculares de la Celula, Facultad de Ciencias y Farmacéuticas, Universidad de Chile, Santiago, Chile.AbstractIn the heart, insulin-like growth factor-1 (IGF-1) is a peptide with pro-hypertrophic and anti-apoptotic actions. The pro-hypertrophic properties of IGF-1 have been attributed to the extracellular regulated kinase (ERK) pathway. Recently, we reported that IGF-1 also increases intracellular Ca(2+) levels through a pertussis toxin (PTX)-sensitive G protein. Here we investigate whether this Ca(2+) signal is involved in IGF-1-induced cardiomyocyte hypertrophy. Our results show that the IGF-1-induced increase in Ca(2+) level is abolished by the IGF-1 receptor tyrosine kinase inhibitor AG538, PTX and the peptide inhibitor of Gβγ signaling, βARKct. Increases in the activities of Ca(2+) -dependent enzymes calcineurin, calmodulin kinase II (CaMKII), and protein kinase Cα (PKCα) were observed at 5 min after IGF-1 exposure. AG538, PTX, βARKct, and the dominant negative PKCα prevented the IGF-1-dependent phosphorylation of ERK1/2. Participation of calcineurin and CaMKII in ERK phosphorylation was discounted. IGF-1-induced cardiomyocyte hypertrophy, determined by cell size and β-myosin heavy chain (β-MHC), was prevented by AG538, PTX, βARKct, dominant negative PKCα, and the MEK1/2 inhibitor PD98059. Inhibition of calcineurin with CAIN did not abolish IGF-1-induced cardiac hypertrophy. We conclude that IGF-1 induces hypertrophy in cultured cardiomyocytes by activation of the receptor tyrosine kinase activity/βγ-subunits of a PTX-sensitive G protein/Ca(2+) /PKCα/ERK pathway without the participation of calcineurin. J. Cell. Biochem. 115: 712-720, 2014. © 2013 Wiley Periodicals, Inc.
- Journal of cellular biochemistry.J Cell Biochem.2014 Apr;115(4):712-20. doi: 10.1002/jcb.24712.
- In the heart, insulin-like growth factor-1 (IGF-1) is a peptide with pro-hypertrophic and anti-apoptotic actions. The pro-hypertrophic properties of IGF-1 have been attributed to the extracellular regulated kinase (ERK) pathway. Recently, we reported that IGF-1 also increases intracellular Ca(2+) le
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