FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1988035682> ?p ?o ?g. }

• W1988035682 endingPage "1943" @default.
• W1988035682 startingPage "1927" @default.
• W1988035682 abstract "In hypertension, an increase in arterial wall thickness and loss of elasticity over time result in an increase in pulse wave velocity, a direct measure of arterial stiffness. This change is reflected in gradual fragmentation and loss of elastin fibers and accumulation of stiffer collagen fibers in the media that occurs independently of atherosclerosis. Similar results are seen with an elevated level of homocysteine (Hcy), known as hyperhomocysteinemia (HHcy), which increases vascular thickness, elastin fragmentation, and arterial blood pressure. Studies from our laboratory have demonstrated a decrease in elasticity and an increase in pulse wave velocity in HHcy cystathionine β synthase heterozygote knockout (CBS−/+) mice. Nitric oxide (NO) is a potential regulator of matrix metalloproteinase (MMP) activity in MMP-NO-TIMP (tissue inhibitor of metalloproteinase) inhibitory tertiary complex. We have demonstrated the contribustion of the NO synthase (NOS) isoforms, endothelial NOS and inducible NOS, in the activation of latent MMP. The differential production of NO contributes to oxidative stress and increased oxidative/nitrative activation of MMP resulting in vascular remodeling in response to HHcy. The contribution of the NOS isoforms, endothelial and inducible in the collagen/elastin switch, has been demonstrated. We have showed that an increase in inducible NOS activity is a key contributor to HHcy-mediated collagen/elastin switch and resulting decline in aortic compliance. In addition, increased levels of Hcy compete and suppress the γ-amino butyric acid-receptor, N-methyl-d-aspartate-receptor, and peroxisome proliferator-activated receptor. The HHcy causes oxidative stress by generating nitrotyrosine, activating the latent MMPs and decreasing the endothelial NO concentration. The HHcy causes elastinolysis and decrease elastic complicance of the vessel wall. The treatment with γ-amino butyric acid-receptor agonist (muscimol), N-methyl-d-aspartate-receptor antagonist (MK-801), and peroxisome proliferator-activated receptor agonists (ciprofibrate and ciglitazone) mitigates the cardiovascular dysfunction in HHcy. Antioxid. Redox Signal. 15, 1927–1943." @default.
• W1988035682 created "2016-06-24" @default.
• W1988035682 creator A5003454740 @default.
• W1988035682 creator A5028741190 @default.
• W1988035682 date "2011-10-01" @default.
• W1988035682 modified "2023-10-18" @default.
• W1988035682 title "Mechanisms of Cardiovascular Remodeling in Hyperhomocysteinemia" @default.
• W1988035682 cites W1513696494 @default.
• W1988035682 cites W1525040400 @default.
• W1988035682 cites W1557154008 @default.
• W1988035682 cites W1605154757 @default.
• W1988035682 cites W1951207992 @default.
• W1988035682 cites W1966292733 @default.
• W1988035682 cites W1974358158 @default.
• W1988035682 cites W1977328014 @default.
• W1988035682 cites W1977841860 @default.
• W1988035682 cites W1978290051 @default.
• W1988035682 cites W1978470738 @default.
• W1988035682 cites W1982556373 @default.
• W1988035682 cites W2007242048 @default.
• W1988035682 cites W2007354513 @default.
• W1988035682 cites W2011302251 @default.
• W1988035682 cites W2015312591 @default.
• W1988035682 cites W2022699060 @default.
• W1988035682 cites W2025782661 @default.
• W1988035682 cites W2026305011 @default.
• W1988035682 cites W2026654109 @default.
• W1988035682 cites W2027385056 @default.
• W1988035682 cites W2027607346 @default.
• W1988035682 cites W2027665192 @default.
• W1988035682 cites W2035620169 @default.
• W1988035682 cites W2039983719 @default.
• W1988035682 cites W2041553504 @default.
• W1988035682 cites W2041615795 @default.
• W1988035682 cites W2051061580 @default.
• W1988035682 cites W2054115147 @default.
• W1988035682 cites W2057397662 @default.
• W1988035682 cites W2066992394 @default.
• W1988035682 cites W2068653999 @default.
• W1988035682 cites W2078410199 @default.
• W1988035682 cites W2081460705 @default.
• W1988035682 cites W2087365405 @default.
• W1988035682 cites W2089580499 @default.
• W1988035682 cites W2090685111 @default.
• W1988035682 cites W2091219676 @default.
• W1988035682 cites W2094025155 @default.
• W1988035682 cites W2096762235 @default.
• W1988035682 cites W2099821538 @default.
• W1988035682 cites W2103257623 @default.
• W1988035682 cites W2105265142 @default.
• W1988035682 cites W2105508112 @default.
• W1988035682 cites W2105900224 @default.
• W1988035682 cites W2107818859 @default.
• W1988035682 cites W2108484297 @default.
• W1988035682 cites W2111899435 @default.
• W1988035682 cites W2112773909 @default.
• W1988035682 cites W2115276193 @default.
• W1988035682 cites W2116164680 @default.
• W1988035682 cites W2118015493 @default.
• W1988035682 cites W2122453286 @default.
• W1988035682 cites W2126736296 @default.
• W1988035682 cites W2132780908 @default.
• W1988035682 cites W2137570167 @default.
• W1988035682 cites W2137738179 @default.
• W1988035682 cites W2145734151 @default.
• W1988035682 cites W2146648547 @default.
• W1988035682 cites W2151482800 @default.
• W1988035682 cites W2152013587 @default.
• W1988035682 cites W2154084777 @default.
• W1988035682 cites W2156158060 @default.
• W1988035682 cites W2156588431 @default.
• W1988035682 cites W2156997639 @default.
• W1988035682 cites W2159495338 @default.
• W1988035682 cites W2164646258 @default.
• W1988035682 cites W2164721380 @default.
• W1988035682 cites W2165884492 @default.
• W1988035682 cites W2168595038 @default.
• W1988035682 cites W2239717990 @default.
• W1988035682 cites W2275754619 @default.
• W1988035682 cites W2394989810 @default.
• W1988035682 cites W244700151 @default.
• W1988035682 cites W3175048990 @default.
• W1988035682 cites W4212986840 @default.
• W1988035682 cites W4241703202 @default.
• W1988035682 cites W53643753 @default.
• W1988035682 doi "https://doi.org/10.1089/ars.2010.3721" @default.
• W1988035682 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3159179" @default.
• W1988035682 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21126196" @default.
• W1988035682 hasPublicationYear "2011" @default.
• W1988035682 type Work @default.
• W1988035682 sameAs 1988035682 @default.
• W1988035682 citedByCount "146" @default.
• W1988035682 countsByYear W19880356822012 @default.
• W1988035682 countsByYear W19880356822013 @default.
• W1988035682 countsByYear W19880356822014 @default.
• W1988035682 countsByYear W19880356822015 @default.
• W1988035682 countsByYear W19880356822016 @default.
• W1988035682 countsByYear W19880356822017 @default.

• next