Antifibrotic effects of N-acetyl-seryl-aspartyl-Lysyl-proline on the heart and kidney in aldosterone-salt hypertensive rats.
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A modern understanding of the traditional and nontraditional biological functions of angiotensin-converting enzymeN-acetyl-seryl-aspartyl-lysyl-proline prevents cardiac remodeling and dysfunction induced by galectin-3, a mammalian adhesion/growth-regulatory lectinHepatoprotective and Anti-fibrotic Agents: It's Time to Take the Next StepN-acetyl-seryl-aspartyl-lysyl-proline: a valuable endogenous anti-fibrotic peptide for combating kidney fibrosis in diabetesACE inhibitors: a novel treatment for neurofibromaDifferential effects of 17beta-estradiol and of synthetic progestins on aldosterone-salt-induced kidney diseaseThe expression levels of prolyl oligopeptidase responds not only to neuroinflammation but also to systemic inflammation upon liver failure in rat models and cirrhotic patientsTRB3 gene silencing alleviates diabetic cardiomyopathy in a type 2 diabetic rat modelN-acetyl-seryl-aspartyl-lysyl-proline attenuates renal injury and dysfunction in hypertensive rats with reduced renal mass: council for high blood pressure researchAc-SDKP inhibits transforming growth factor-beta1-induced differentiation of human cardiac fibroblasts into myofibroblasts.Myocardial regeneration: expanding the repertoire of thymosin β4 in the ischemic heartEffects of exogenous thymosin β4 on carbon tetrachloride-induced liver injury and fibrosisN-acetyl-Ser-Asp-Lys-Pro inhibits interleukin-1β-mediated matrix metalloproteinase activation in cardiac fibroblasts.N-acetyl-seryl-aspartyl-lysyl-proline reduces cardiac collagen cross-linking and inflammation in angiotensin II-induced hypertensive ratsA novel angiotensin I-converting enzyme mutation (S333W) impairs N-domain enzymatic cleavage of the anti-fibrotic peptide, AcSDKP.Prolyl oligopeptidase induces angiogenesis both in vitro and in vivo in a novel regulatory manner.N-Acetyl-Seryl-Aspartyl-Lysyl-Proline: mechanisms of renal protection in mouse model of systemic lupus erythematosusRole of N-acetyl-seryl-aspartyl-lysyl-proline in the antifibrotic and anti-inflammatory effects of the angiotensin-converting enzyme inhibitor captopril in hypertensionNontraditional roles of angiotensin-converting enzyme.N-Acetyl-seryl-aspartyl-lysyl-proline Alleviates Renal Fibrosis Induced by Unilateral Ureteric Obstruction in BALB/C Mice.N-Acetyl-seryl-aspartyl-lysyl-proline inhibits ET-1-induced collagen production by preserving Src homology 2-containing protein tyrosine phosphatase-2 activity in cardiac fibroblasts.Treatment with N-acetyl-seryl-aspartyl-lysyl-proline prevents experimental autoimmune myocarditis in ratsCharacterization and localization of Ac-SDKP receptor binding sites using 125I-labeled Hpp-Aca-SDKP in rat cardiac fibroblastsPrevention of aortic fibrosis by N-acetyl-seryl-aspartyl-lysyl-proline in angiotensin II-induced hypertension.Ramipril attenuates left ventricular remodeling by regulating the expression of activin A-follistatin in a rat model of heart failureThymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis.Effects of N-acetyl-seryl-asparyl-lysyl-proline on blood pressure, renal damage, and mortality in systemic lupus erythematosusCombination treatment with N-acetyl-seryl-aspartyl-lysyl-proline and tissue plasminogen activator provides potent neuroprotection in rats after strokeElevation of the antifibrotic peptide N-acetyl-seryl-aspartyl-lysyl-proline: a blood pressure-independent beneficial effect of angiotensin I-converting enzyme inhibitorsPathophysiology of the aging kidney and therapeutic interventions.Antifibrotic peptide N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP): opportunities for angiotensin-converting enzyme inhibitor design.The biological significance of angiotensin-converting enzyme inhibition to combat kidney fibrosis.Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction.N-acetyl-seryl-aspartyl-lysyl-proline stimulates angiogenesis in vitro and in vivo.Renal protective effects of N-acetyl-Ser-Asp-Lys-Pro in deoxycorticosterone acetate-salt hypertensive miceProlyl oligopeptidase is involved in release of the antifibrotic peptide Ac-SDKP.Ac-SDKP suppresses TNF-α-induced ICAM-1 expression in endothelial cells via inhibition of IκB kinase and NF-κB activation.Treatment of traumatic brain injury in rats with N-acetyl-seryl-aspartyl-lysyl-proline.The role of Na+-H+ exchanger isoform 1 in aldosterone-induced glomerulosclerosis in vivo.A role for cardiotrophin-1 in myocardial remodeling induced by aldosterone.
P2860
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P2860
Antifibrotic effects of N-acetyl-seryl-aspartyl-Lysyl-proline on the heart and kidney in aldosterone-salt hypertensive rats.
description
2001 nî lūn-bûn
@nan
2001 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Antifibrotic effects of N-acet ...... terone-salt hypertensive rats.
@ast
Antifibrotic effects of N-acet ...... terone-salt hypertensive rats.
@en
type
label
Antifibrotic effects of N-acet ...... terone-salt hypertensive rats.
@ast
Antifibrotic effects of N-acet ...... terone-salt hypertensive rats.
@en
prefLabel
Antifibrotic effects of N-acet ...... terone-salt hypertensive rats.
@ast
Antifibrotic effects of N-acet ...... terone-salt hypertensive rats.
@en
P2093
P356
P1433
P1476
Antifibrotic effects of N-acet ...... sterone-salt hypertensive rats
@en
P2093
P304
P356
10.1161/01.HYP.37.2.794
P407
P433
P577
2001-02-01T00:00:00Z