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Coronary Artery Disease: HELP
Articles by Timothy C. Nichols
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, T. C. Nichols wrote the following 3 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Article Coronary Artery Disease Risk-Associated 2019

Mueller, Paul A / Yang, Liping / Ubele, Margo / Mao, Guogen / Brandon, Jason / Vandra, Julia / Nichols, Timothy C / Escalante-Alcalde, Diana / Morris, Andrew J / Smyth, Susan S. ·From the Division of Cardiovascular Medicine, The Gill Heart & Vascular Institute, University of Kentucky, Lexington (P.A.M., L.Y., M.U., G.M., J.B., J.V., A.J.M., S.S.S.). · Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill (T.C.N.). · División de Neurociencias, Instituto de Fisiología, Celular Universidad Nacional Autónoma de México, Ciudad de México, CDMX (D.E.-A.). · Department of Veterans Affairs Medical Center, Lexington, KY (A.J.M., S.S.S.). ·Arterioscler Thromb Vasc Biol · Pubmed #31533471.

ABSTRACT: OBJECTIVE: Genome-wide association studies identified novel loci in CONCLUSIONS: Our results identify a novel lipid signaling pathway that regulates inflammation in the context of atherosclerosis and is not related to traditional risk factors. Pharmacological targeting of bioactive LPP3 substrates, including LPA, may offer an orthogonal approach to lipid-lowering drugs for mitigation of coronary artery disease risk.

2 Article An anti-αVβ3 antibody inhibits coronary artery atherosclerosis in diabetic pigs. 2017

Maile, L A / Busby, W H / Xi, G / Gollahan, K P / Flowers, W / Gafbacik, N / Gafbacik, S / Stewart, K / Merricks, E P / Nichols, T C / Bellinger, D A / Clemmons, D R. ·Department of Medicine, UNC School of Medicine, Chapel Hill, NC, USA. · Department of Animal Science, NC State University, Raleigh, NC, USA. · Department of Medicine, UNC School of Medicine, Chapel Hill, NC, USA. Electronic address: endo@med.unc.edu. ·Atherosclerosis · Pubmed #28189040.

ABSTRACT: BACKGROUND AND AIMS: Diabetes is a major risk factor for the development of atherosclerosis. Hyperglycemia stimulates vascular smooth muscle cells (VSMC) to secrete ligands that bind to the αVβ3 integrin, a receptor that regulates VSMC proliferation and migration. This study determined whether an antibody that had previously been shown to block αVβ3 activation and to inhibit VSMC proliferation and migration in vitro, inhibited the development of atherosclerosis in diabetic pigs. METHODS: Twenty diabetic pigs were maintained on a high fat diet for 22 weeks. Ten received injections of anti-β3 F(ab) RESULTS: The active antibody group showed reduction of atherosclerosis of 91 ± 9% in the left main, 71 ± 11%, in left anterior descending, 80 ± 10.2% in circumflex, and 76 ± 25% in right coronary artery, (p < 0.01 compared to lesions areas from corresponding control treated arteries). There were significant reductions in both cell number and extracellular matrix. Histologic analysis showed neointimal hyperplasia with macrophage infiltration, calcifications and cholesterol clefts. Antibody treatment significantly reduced number of macrophages contained within lesions, suggesting that this change contributed to the decrease in lesion cellularity. Analysis of the biochemical changes within the femoral arteries that received the active antibody showed a 46 ± 12% (p < 0.05) reduction in the tyrosine phosphorylation of the β3 subunit of αVβ3 and a 40 ± 14% (p < 0.05) reduction in MAP kinase activation. CONCLUSIONS: Blocking ligand binding to the αVβ3 integrin inhibits its activation and attenuates increased VSMC proliferation that is induced by chronic hyperglycemia. These changes result in significant decreases in atherosclerotic lesion size in the coronary arteries. The results suggest that this approach may have efficacy in treating the proliferative phase of atherosclerosis in patients with diabetes.

3 Article Oxidized LDL and Fructosamine Associated with Severity of Coronary Artery Atherosclerosis in Insulin Resistant Pigs Fed a High Fat/High NaCl Diet. 2015

Nichols, Timothy C / Merricks, Elizabeth P / Bellinger, Dwight A / Raymer, Robin A / Yu, Jing / Lam, Diana / Koch, Gary G / Busby, Walker H / Clemmons, David R. ·Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. · Department of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. · Department of Biostatistics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. · Department of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. ·PLoS One · Pubmed #26147990.

ABSTRACT: BACKGROUND: Insulin-resistant subjects develop more severe and diffuse coronary artery atherosclerosis than insulin-sensitive controls but the mechanisms that mediate this atherosclerosis phenotype are unknown. RESEARCH OBJECTIVE: To determine the metabolic parameters that associate with the severity of coronary atherosclerosis in insulin resistant pigs fed a high fat/high NaCl diet. KEY METHODS: The primary endpoint was severity of coronary atherosclerosis in adult pigs (Sus scrofa, n = 37) fed a high fat diet that also contained high NaCl (56% above recommended levels) for 1 year. PRINCIPAL FINDINGS: Twenty pigs developed severe and diffuse distal coronary artery atherosclerosis (i.e., severe = intimal area as a percent medial area > 200% in at least 2 coronary artery cross sections and diffuse distal = intimal area as a percent medial area ≥ 150% over 3 sections separated by 2 cm in the distal half of the coronary artery). The other 17 pigs had substantially less coronary artery atherosclerosis. All 37 pigs had blood pressure in a range that would be considered hypertensive in humans and developed elevations in total and LDL and HDL cholesterol, weight gain, increased backfat, and increased insulin resistance (Bergman Si) without overt diabetes. Insulin resistance was not associated with atherosclerosis severity. Five additional pigs fed regular pig chow also developed increased insulin resistance but essentially no change in the other variables and little to no detectible coronary atherosclerosis. Most importantly, the 20 high fat/high NaCl diet-fed pigs with severe and diffuse distal coronary artery atherosclerosis had substantially greater increases (p< 0.05) in oxidized LDL (oxLDL) and fructosamine consistent with increased protein glycation. CONCLUSION: In pigs fed a high fat/high NaCl diet, glycated proteins are induced in the absence of overt diabetes and this degree of increase is associated with the development of severe and diffuse distal coronary artery atherosclerosis.