| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Irina Rudik Miksa, Margaret R Cummings, Robert H Poppeng. Multi-residue determination of anti-inflammatory analgesics in sera by liquid chromatography--mass spectrometry. Journal of analytical toxicology. vol 29. issue 2. 2005-09-01. PMID:15902977. |
the matrix lods were determined to be 0.05 microg/ml for phenylbutazone (m/z 307); 0.1 microg/ml for indomethacin (m/z 312), flunixin (m/z 295), and piroxicam (m/z 330); 0.5 microg/ml for ace (m/z 150), diclofenac (m/z 250), ketoprofen (m/z 209), and mefenamic acid (m/z 240); 1.0 microg/ml for oxyphenbutazone (m/z 323); 5.0 microg/ml for ibuprofen (m/z 205), salicylic acid (m/z 137), and tolmetin (m/z 212); and 10 microg/ml for naproxen (m/z 185). |
2005-09-01 |
2023-08-12 |
human |
| Martin Liebetrau, Dorothe Burggraf, Nathalie Wunderlich, Gabriele Jäger, Wolfgang Linz, Gerhard F Haman. ACE inhibition reduces activity of the plasminogen/plasmin and MMP systems in the brain of spontaneous hypertensive stroke-prone rats. Neuroscience letters. vol 376. issue 3. 2005-05-26. PMID:15721222. |
these findings provide new insights into the biochemical mechanisms underlying extracellular matrix proliferation and its modulation by ace inhibitors. |
2005-05-26 |
2023-08-12 |
rat |
| Kazuyuki Shibuya, Keizo Kanasaki, Motohide Isono, Haruhisa Sato, Mitsugu Omata, Toshiro Sugimoto, Shin-ichi Araki, Keiji Isshiki, Atsunori Kashiwagi, Masakazu Haneda, Daisuke Koy. N-acetyl-seryl-aspartyl-lysyl-proline prevents renal insufficiency and mesangial matrix expansion in diabetic db/db mice. Diabetes. vol 54. issue 3. 2005-04-22. PMID:15734863. |
we have previously reported that n-acetyl-seryl-aspartyl-lysyl-proline (ac-sdkp), which is a tetrapeptide hydrolyzed by ace, inhibits the transforming growth factor-beta (tgf-beta)-induced expression of extracellular matrix proteins via inhibition of the smad signaling in human mesangial cells. |
2005-04-22 |
2023-08-12 |
mouse |
| Yovani Marrero Ponce, Humberto González Diaz, Vicente Romero Zaldivar, Francisco Torrens, Eduardo A Castr. 3D-chiral quadratic indices of the 'molecular pseudograph's atom adjacency matrix' and their application to central chirality codification: classification of ACE inhibitors and prediction of sigma-receptor antagonist activities. Bioorganic & medicinal chemistry. vol 12. issue 20. 2005-03-11. PMID:15388160. |
3d-chiral quadratic indices of the 'molecular pseudograph's atom adjacency matrix' and their application to central chirality codification: classification of ace inhibitors and prediction of sigma-receptor antagonist activities. |
2005-03-11 |
2023-08-12 |
Not clear |
| Hirokazu Okada, Yusuke Watanabe, Tomohiro Kikuta, Tatsuya Kobayashi, Yoshihiko Kanno, Takeshi Sugaya, Hiromichi Suzuk. Bradykinin decreases plasminogen activator inhibitor-1 expression and facilitates matrix degradation in the renal tubulointerstitium under angiotensin-converting enzyme blockade. Journal of the American Society of Nephrology : JASN. vol 15. issue 9. 2005-02-22. PMID:15339989. |
in this murine model of csa nephropathy under ace blockade, plasminogen activator inhibitor-1 (pai-1) expression was decreased in tubular epithelial cells, possibly leading to conversion of plasminogen to plasmin by plasminogen activator and subsequent activation of matrix metalloproteinases. |
2005-02-22 |
2023-08-12 |
Not clear |
| Thomas Unger, Jun L. The role of the renin-angiotensin-aldosterone system in heart failure. Journal of the renin-angiotensin-aldosterone system : JRAAS. vol 5 Suppl 1. 2005-02-15. PMID:15526242. |
chymase, a protease inhibitor stored in mast cells that generates angiotensin ii (ang ii) (in addition to angiotensin-converting enzyme [ace]), has been linked to extracellular matrix remodelling in heart failure. |
2005-02-15 |
2023-08-12 |
Not clear |
| Damiano Rizzoni, Gian Paolo Rossi, Enzo Porteri, Daniele Sticchi, Luigi Rodella, Rita Rezzani, Intissar Sleiman, Carolina De Ciuceis, Silvia Paiardi, Rossella Bianchi, G G Nussdorfer, Enrico Agabiti-Rose. Bradykinin and matrix metalloproteinases are involved the structural alterations of rat small resistance arteries with inhibition of ACE and NEP. Journal of hypertension. vol 22. issue 4. 2004-12-06. PMID:15126918. |
bradykinin and matrix metalloproteinases are involved the structural alterations of rat small resistance arteries with inhibition of ace and nep. |
2004-12-06 |
2023-08-12 |
rat |
| Yasushi Sakata, Kazuhiro Yamamoto, Toshiaki Mano, Nagahiro Nishikawa, Junichi Yoshida, Masatsugu Hori, Takeshi Miwa, Tohru Masuyam. Activation of matrix metalloproteinases precedes left ventricular remodeling in hypertensive heart failure rats: its inhibition as a primary effect of Angiotensin-converting enzyme inhibitor. Circulation. vol 109. issue 17. 2004-09-10. PMID:15051632. |
matrix metalloproteinases (mmps) are activated in dilated failing hearts, and angiotensin-converting enzyme (ace) inhibition prevents left ventricular (lv) dilatation. |
2004-09-10 |
2023-08-12 |
rat |
| Jürgen Scholz. [Pulse pressure in the therapeutic management of hypertension?]. Herz. vol 29. issue 3. 2004-08-11. PMID:15167954. |
antihypertensive drugs may improve vascular compliance and the alterations of microvascular architecture by reducing blood pressure, relaxing vascular smooth muscle, or promoting long-term effects on extracellular matrix, collagen, vascular smooth muscle, and cardiomyocyte growth and remodeling.diuretics, beta blockers, long-acting calcium channel blockers, angiotensin-converting enzyme (ace) inhibitors and angiotensin i (at(1)) receptor antagonists were critically discussed in relation to their influence on vascular compliance, endothelial dysfunction, the remodeling process, pp, and cardiovascular morbidity and mortality. |
2004-08-11 |
2023-08-12 |
Not clear |
| Pamela Harding, William F Glass, Steven D Schere. COX-2 inhibition potentiates the antiproteinuric effect of enalapril in uninephrectomized SHR. Prostaglandins, leukotrienes, and essential fatty acids. vol 68. issue 1. 2004-04-26. PMID:12538086. |
pge(2) and pgi(2) reduce extracellular matrix deposition and their production is altered after ace inhibitor (acei) treatment. |
2004-04-26 |
2023-08-12 |
Not clear |
| Damiano Rizzoni, Luigi Rodella, Enzo Porteri, Rita Rezzani, Intissar Sleiman, Silvia Paiardi, Daniele Guelfi, Carolina De Ciuceis, Gianluca E M Boari, Rossella Bianchi, Enrico Agabiti-Rose. Effects of losartan and enalapril at different doses on cardiac and renal interstitial matrix in spontaneously hypertensive rats. Clinical and experimental hypertension (New York, N.Y. : 1993). vol 25. issue 7. 2004-02-02. PMID:14596367. |
in conclusion, los and ena showed a similar preventive effect on the increase of rlvm in shr, but, at least in part, different effects on the extracellular matrix in different organs, being cardiac collagen less sensitive to low dose (ld) ace inhibition. |
2004-02-02 |
2023-08-12 |
rat |
| Xiao R Huang, Wei Y Chen, Luan D Truong, Hui Y La. Chymase is upregulated in diabetic nephropathy: implications for an alternative pathway of angiotensin II-mediated diabetic renal and vascular disease. Journal of the American Society of Nephrology : JASN. vol 14. issue 7. 2003-08-19. PMID:12819233. |
in the diabetic kidney, while ace expression was significantly upregulated (1 to 3-fold) by tubular epithelial cells (tec) and infiltrating mononuclear cells, there was also markedly increased chymase expression (10 to 15-fold) by both mc and vsmc, with strong deposition in the collagen-rich extracellular matrix including both diffuse and nodular glomerulosclerosis, tubulointerstitial fibrosis, and vascular sclerosis. |
2003-08-19 |
2023-08-12 |
human |
| Xiao R Huang, Wei Y Chen, Luan D Truong, Hui Y La. Chymase is upregulated in diabetic nephropathy: implications for an alternative pathway of angiotensin II-mediated diabetic renal and vascular disease. Journal of the American Society of Nephrology : JASN. vol 14. issue 7. 2003-08-19. PMID:12819233. |
correlation analysis showed that, in contrast to the ace expression, upregulation of chymase correlated significantly with the increase in bp and the severity of collagen matrix deposition within the glomerulus, tubulointerstitium, and arterial walls (all with p < 0.001). |
2003-08-19 |
2023-08-12 |
human |
| Mingyi Wang, Gen Takagi, Kuniya Asai, Ranilo G Resuello, Filipinas F Natividad, Dorothy E Vatner, Stephen F Vatner, Edward G Lakatt. Aging increases aortic MMP-2 activity and angiotensin II in nonhuman primates. Hypertension (Dallas, Tex. : 1979). vol 41. issue 6. 2003-06-27. PMID:12743015. |
to seek evidence that the nonhuman primate arterial wall, as it ages in the absence of atherosclerosis, exhibits alterations in pathways that are involved in the pathogenesis of experimental atherosclerosis, we assessed aortic matrix metalloproteinase-2 (mmp-2) and its regulators, ie, membrane type-1 of matrix metalloproteinase (mt1-mmp) and tissue inhibitor of matrix metalloproteinase-2 (timp-2), and the expression of angiotensin ii (ang ii), angiotensin-converting enzyme (ace), and chymase in young (6.4+/-0.7 years) and old (20.0+/-1.9 years) male monkeys. |
2003-06-27 |
2023-08-12 |
monkey |
| Mingyi Wang, Gen Takagi, Kuniya Asai, Ranilo G Resuello, Filipinas F Natividad, Dorothy E Vatner, Stephen F Vatner, Edward G Lakatt. Aging increases aortic MMP-2 activity and angiotensin II in nonhuman primates. Hypertension (Dallas, Tex. : 1979). vol 41. issue 6. 2003-06-27. PMID:12743015. |
with advancing age, (1) the intimal thickness increased 3-fold and contained numerous vascular smooth muscle cells and matrix, but no inflammatory cells; (2) the intimal mmp-2 antibody-staining fraction increased by 80% (p<0.01); (3) in situ zymography showed that mmp-2 activity, mainly confined to the intima, increased 3-fold (p<0.01); (4) the mt1-mmp antibody-staining fraction increased by 150% (p<0.001), but the timp-2 antibody-staining fraction did not significantly change; (5) steady levels of the mrna-staining fraction (via in situ hybridization) for mmp-2 increased 7-fold, for mt1-mmp increased 9-fold, and for timp-2 increased 2-fold (all p<0.001); and (6) intimal ang ii and ace immunofluorescence were increased 5-fold and 5.6-fold, respectively, and colocalized with mmp-2. |
2003-06-27 |
2023-08-12 |
monkey |
| Yasuhisa Kurog. Mesangial cell proliferation inhibitors for the treatment of proliferative glomerular disease. Medicinal research reviews. vol 23. issue 1. 2003-05-28. PMID:12424751. |
it is also known that the mc proliferation is inhibited by many kinds of pharmacological drugs, for example, angiotensin converting enzyme (ace) inhibitors, leukotriene d(4) (ltd(4)) antagonists, pdgf inhibitors, matrix metalloproteinases (mmp) inhibitors, 3-hydroxy-3 methyl glutaryl-coenzymea (hmg-coa) inhibitors, cyclin-dependent kinases (cdk) inhibitors, and others. |
2003-05-28 |
2023-08-12 |
Not clear |
| Boris Chertin, Valeria Solari, Denis J Reen, Amicur Farkas, Prem Pur. Up-regulation of angiotensin-converting enzyme (ACE) gene expression induces tubulointerstitial injury in reflux nephropathy. Pediatric surgery international. vol 18. issue 7. 2003-05-06. PMID:12471481. |
recent studies have suggested that ace increases production of the components of extracellular matrix (ecm) such as fibronectin (fib) mediated through ang ii. |
2003-05-06 |
2023-08-12 |
Not clear |
| D Reinhardt, H H Sigusch, J Hensse, S C Tyagi, R Körfer, H R Figull. Cardiac remodelling in end stage heart failure: upregulation of matrix metalloproteinase (MMP) irrespective of the underlying disease, and evidence for a direct inhibitory effect of ACE inhibitors on MMP. Heart (British Cardiac Society). vol 88. issue 5. 2002-12-09. PMID:12381651. |
cardiac remodelling in end stage heart failure: upregulation of matrix metalloproteinase (mmp) irrespective of the underlying disease, and evidence for a direct inhibitory effect of ace inhibitors on mmp. |
2002-12-09 |
2023-08-12 |
Not clear |
| D Reinhardt, H H Sigusch, J Hensse, S C Tyagi, R Körfer, H R Figull. Cardiac remodelling in end stage heart failure: upregulation of matrix metalloproteinase (MMP) irrespective of the underlying disease, and evidence for a direct inhibitory effect of ACE inhibitors on MMP. Heart (British Cardiac Society). vol 88. issue 5. 2002-12-09. PMID:12381651. |
to investigate matrix metalloproteinases (mmp-2 and mmp-9) in heart failure caused by ischaemic and idiopathic dilated cardiomyopathy, and the impact of angiotensin converting enzyme (ace) inhibition on mmp. |
2002-12-09 |
2023-08-12 |
Not clear |
| Doina Popov, Gabriela Costache, Adriana Georgescu, Mirela Enach. Beneficial effects of L-arginine supplementation in experimental hyperlipemia-hyperglycemia in the hamster. Cell and tissue research. vol 308. issue 1. 2002-09-06. PMID:12012211. |
the results showed that oral supplementation with l-arginine in simultaneous hyperlipemia-hyperglycemia induced in hamsters had favorable effects on: (1) homeostasis, i.e., diminished the concentration of circulating glucose (by ~63%) and cholesterol (by approximately 10%), reduced the ace activity (by approximately 45%), and lowered the osmotic fragility of erythrocyte plasmalemma (as marker for the oxidative stress in plasma); (2) mesenteric resistance arteries, which showed (in 10(-4) m ach) an improved endothelium-dependent relaxation (72.40+/-4.6% in the hd + l-arg group vs 61.90+/-1.45% in the hd group) and a reduced thickness (approximately 1.32-fold) of the smooth muscle cells' extracellular matrix; and (3) the heart, which displayed approximately 16% diminishing of the thickness of the left ventricular wall, and an apparently normal structure of the myocardium; the restoration of the thickness of the pericapillary extracellular matrix to almost normal dimensions was also observed. |
2002-09-06 |
2023-08-12 |
Not clear |