All Relations between hypertrophic and matrix compartment

Publication Sentence Publish Date Extraction Date Species
Y Ogawa, N Tamura, H Chusho, K Naka. Brain natriuretic peptide appears to act locally as an antifibrotic factor in the heart. Canadian journal of physiology and pharmacology. vol 79. issue 8. 2002-02-07. PMID:11558681. in addition to cardiac myocyte hypertrophy, proliferation and increased extracellular matrix production of cardiac fibroblasts occur in response to cardiac overload. 2002-02-07 2023-08-12 mouse
S Beavan, A Horner, S Bord, D Ireland, J Compsto. Colocalization of glucocorticoid and mineralocorticoid receptors in human bone. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. vol 16. issue 8. 2002-01-30. PMID:11499872. in the neonatal rib cartilage, staining for gralpha, gralphabeta, and mr was present in approximately one-half of the resting and hypertrophic chondrocytes and in most of proliferating chondrocytes and chondrocytes within the mineralizing matrix. 2002-01-30 2023-08-12 human
S L Felisbino, H F Carvalh. Growth cartilage calcification and formation of bone trabeculae are late and dissociated events in the endochondral ossification of Rana catesbeiana. Cell and tissue research. vol 306. issue 2. 2002-01-22. PMID:11702243. in stage-46 tadpoles and 1-year-old animals, the hypertrophic cartilage had a smooth contact with the bone marrow and the matrix showed no calcification or endochondral bone formation. 2002-01-22 2023-08-12 Not clear
S L Felisbino, H F Carvalh. Growth cartilage calcification and formation of bone trabeculae are late and dissociated events in the endochondral ossification of Rana catesbeiana. Cell and tissue research. vol 306. issue 2. 2002-01-22. PMID:11702243. calcium deposits appeared as isolated or coalesced spherical structures in the extracellular matrix of hypertrophic cartilage. 2002-01-22 2023-08-12 Not clear
A Schubert, T Walther, V Falk, C Binner, N Löscher, A Kanev, S Bleiziffer, T Rauch, R Autschbach, F W Moh. Extracellular matrix gene expression correlates to left ventricular mass index after surgical induction of left ventricular hypertrophy. Basic research in cardiology. vol 96. issue 4. 2002-01-11. PMID:11518194. extracellular matrix gene expression correlates to left ventricular mass index after surgical induction of left ventricular hypertrophy. 2002-01-11 2023-08-12 Not clear
S Chen, S W Hong, M C Iglesias-de la Cruz, M Isono, A Casaretto, F N Ziyade. The key role of the transforming growth factor-beta system in the pathogenesis of diabetic nephropathy. Renal failure. vol 23. issue 3-4. 2001-12-28. PMID:11499562. prominent among these is transforming growth factor-beta (tgf-beta) because it promotes renal cell hypertrophy and stimulates extracellular matrix accumulation, the two hallmarks of diabetic renal disease. 2001-12-28 2023-08-12 mouse
S Chen, S W Hong, M C Iglesias-de la Cruz, M Isono, A Casaretto, F N Ziyade. The key role of the transforming growth factor-beta system in the pathogenesis of diabetic nephropathy. Renal failure. vol 23. issue 3-4. 2001-12-28. PMID:11499562. neutralizing anti-tgf-beta antibodies prevent the hypertrophic and matrix stimulatory effects of high glucose in these cells. 2001-12-28 2023-08-12 mouse
S Chen, S W Hong, M C Iglesias-de la Cruz, M Isono, A Casaretto, F N Ziyade. The key role of the transforming growth factor-beta system in the pathogenesis of diabetic nephropathy. Renal failure. vol 23. issue 3-4. 2001-12-28. PMID:11499562. we demonstrate that short-term treatment of diabetic mice with neutralizing monoclonal antibodies against tgf-beta significantly reduces kidney weight and glomerular hypertrophy and attenuates the increase in extracellular matrix mrnas. 2001-12-28 2023-08-12 mouse
S Chen, S W Hong, M C Iglesias-de la Cruz, M Isono, A Casaretto, F N Ziyade. The key role of the transforming growth factor-beta system in the pathogenesis of diabetic nephropathy. Renal failure. vol 23. issue 3-4. 2001-12-28. PMID:11499562. the data we review here strongly support the hypothesis that elevated production or activity of the tgf-beta system mediates diabetic renal hypertrophy and extracellular matrix expansion. 2001-12-28 2023-08-12 mouse
O Jacenko, D Chan, A Franklin, S Ito, C B Underhill, J F Bateman, M R Campbel. A dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice. The American journal of pathology. vol 159. issue 6. 2001-12-18. PMID:11733375. a dominant interference collagen x mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice. 2001-12-18 2023-08-12 mouse
O Jacenko, D Chan, A Franklin, S Ito, C B Underhill, J F Bateman, M R Campbel. A dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice. The American journal of pathology. vol 159. issue 6. 2001-12-18. PMID:11733375. electron microscopy revealed a disrupted hexagonal lattice network in the hypertrophic chondrocyte pericellular matrix in tg growth plates, as well as altered mineral deposition. 2001-12-18 2023-08-12 mouse
S Goldfarb, F N Ziyade. TGF-beta: a crucial component of the pathogenesis of diabetic nephropathy. Transactions of the American Clinical and Climatological Association. vol 112. 2001-12-07. PMID:11413780. increased tgf-beta expression in the kidney in diabetes mellitus mediates the renal actions of high ambient glucose to promote cellular hypertrophy and stimulate extracellular matrix biosynthesis. 2001-12-07 2023-08-12 mouse
F Zannad, B Dousset, F All. Treatment of congestive heart failure: interfering the aldosterone-cardiac extracellular matrix relationship. Hypertension (Dallas, Tex. : 1979). vol 38. issue 5. 2001-12-07. PMID:11711528. cardiac extracellular matrix undergoes extensive and continuous turnover involved in the lesion-reparation process, such as in cardiac remodeling, in hypertensive cardiac hypertrophy, in dilated cardiomyopathy, after myocardial infarction in the transition to heart failure, and during the progression of left ventricular dysfunction. 2001-12-07 2023-08-12 Not clear
J L Gooch, Y Tang, J M Ricono, H E Abbou. Insulin-like growth factor-I induces renal cell hypertrophy via a calcineurin-dependent mechanism. The Journal of biological chemistry. vol 276. issue 45. 2001-12-05. PMID:11509557. igf-i induced hypertrophy as determined by an increase in cell size and an increase in protein to dna ratio and increased accumulation of extracellular matrix (ecm) proteins. 2001-12-05 2023-08-12 Not clear
T Nakase, T Miyaji, K Kuriyama, N Tamai, M Horiki, T Tomita, A Myoui, K Shimada, H Yoshikaw. Immunohistochemical detection of parathyroid hormone-related peptide, Indian hedgehog, and patched in the process of endochondral ossification in the human. Histochemistry and cell biology. vol 116. issue 3. 2001-12-05. PMID:11685558. pthrp, ihh, and ptc were immunolocalized in prehypertrophic and hypertrophic chondrocytes in mature cartilage matrix. 2001-12-05 2023-08-12 human
A J Hayes, S MacPherson, H Morrison, G Dowthwaite, C W Arche. The development of articular cartilage: evidence for an appositional growth mechanism. Anatomy and embryology. vol 203. issue 6. 2001-12-04. PMID:11453164. it is well-established that cartilage grows by a combination of matrix secretion, cell hypertrophy and cell proliferation. 2001-12-04 2023-08-12 Not clear
T Walther, A Schubert, V Falk, C Binner, A Kanev, S Bleiziffer, C Walther, N Doll, R Autschbach, F W Moh. Regression of left ventricular hypertrophy after surgical therapy for aortic stenosis is associated with changes in extracellular matrix gene expression. Circulation. vol 104. issue 12 Suppl 1. 2001-10-04. PMID:11568030. regression of left ventricular hypertrophy after surgical therapy for aortic stenosis is associated with changes in extracellular matrix gene expression. 2001-10-04 2023-08-12 Not clear
V S Mujumdar, L M Smiley, S C Tyag. Activation of matrix metalloproteinase dilates and decreases cardiac tensile strength. International journal of cardiology. vol 79. issue 2-3. 2001-09-27. PMID:11461752. previous studies demonstrated that transition from compensatory pressure overload hypertrophy to decompensatory volume overload heart failure is associated with decreased cardiac tensile strength and activation of matrix metalloproteinase (mmp) in spontaneously hypertensive rat (shr). 2001-09-27 2023-08-12 rat
V S Mujumdar, L M Smiley, S C Tyag. Activation of matrix metalloproteinase dilates and decreases cardiac tensile strength. International journal of cardiology. vol 79. issue 2-3. 2001-09-27. PMID:11461752. to test the hypothesis that in the absence of nitric oxide activation of mmp during cardiac failure causes disruption in the organization of extracellular matrix (ecm) and leads to decrease systolic and diastolic cardiac tensile strength, we employed shr of 24--32 weeks, which demonstrates significant cardiac hypertrophy and fibrosis. 2001-09-27 2023-08-12 rat
V S Mujumdar, L M Smiley, S C Tyag. Activation of matrix metalloproteinase dilates and decreases cardiac tensile strength. International journal of cardiology. vol 79. issue 2-3. 2001-09-27. PMID:11461752. to determine whether cardiac hypertrophy is associated with increased elastinolytic matrix metalloproteinase-2 (mmp-2) activity; quantitative elastin-zymography was performed on cardiac tissue homogenates. 2001-09-27 2023-08-12 rat