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Coronary Artery Disease: HELP
Articles by Diana Escalante-Alcalde
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Diana Escalante-Alcalde wrote the following 2 articles about Coronary Artery Disease.
 
+ Citations + Abstracts
1 Review Lipid phosphate phosphatase 3 in vascular pathophysiology. 2018

Busnelli, Marco / Manzini, Stefano / Parolini, Cinzia / Escalante-Alcalde, Diana / Chiesa, Giulia. ·Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milano, Italy. Electronic address: marco.busnelli@unimi.it. · Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milano, Italy. · Instituto de Fisiología Celular, División de Neurociencias Universidad Nacional Autónoma de México, Cd. Mx., 04510, Mexico. · Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milano, Italy. Electronic address: giulia.chiesa@unimi.it. ·Atherosclerosis · Pubmed #29518748.

ABSTRACT: LPP3 is an integral membrane protein belonging to a family of enzymes (LPPs) that display broad substrate specificity and catalyse dephosphorylation of several lipid substrates, including lysophosphatidic acid and sphingosine-1-phosphate. In mammals, the LPP family consists of three enzymes named LPP1, LPP2 and LPP3, which are encoded by three independent genes, PLPP1, PLPP2 and PLPP3, respectively (formerly known as PPAP2A, PPAP2C, PPAP2B). These three enzymes, in vitro, do not seem to differ for catalytic activities and substrate preferences. However, in vivo targeted inactivation of the individual genes has indicated that the enzymes do not have overlapping functions and that LPP3, specifically, plays a crucial role in vascular development. In 2011, two genome-wide association studies have identified PLPP3 as a novel locus associated with coronary artery disease susceptibility. Shortly after these reports, tissue specific inactivation of PLPP3 in mice highlighted a specific role for LPP3 in vascular pathophysiology and, more recently, in atherosclerosis development. This review is aimed at providing an updated overview on the function of LPP3 in embryonic cardiovascular development and on the experimental and clinical evidences relating this enzyme to vascular cell functions and cardiovascular disease.

2 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.