Acid Sphingomyelinase Promotes Lipoprotein Retention Within Early Atheromata and Accelerates Lesion Progression | Zendy

Cecilia Devlin | Zendy; Andrew Leventhal | Zendy; George Kuriakose | Zendy; Edward H. Schuchman | Zendy; Kevin Jon Williams | Zendy; Ira Tabas | Zendy

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Acid Sphingomyelinase Promotes Lipoprotein Retention Within Early Atheromata and Accelerates Lesion Progression

Author(s) -

Cecilia Devlin,

Andrew Leventhal,

George Kuriakose,

Edward H. Schuchman,

Kevin Jon Williams,

Ira Tabas

Publication year - 2008

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.108.173344

Subject(s) - sphingomyelin , lesion , ceramide , cancer research , lipoprotein , acid sphingomyelinase , biology , medicine , pathology , cholesterol , biochemistry , apoptosis

The key initial step in atherogenesis is the subendothelial retention of apolipoprotein B-containing lipoproteins. Acid sphingomyelinase (acid SMase), an enzyme present extracellularly within the arterial wall, strongly enhances lipoprotein retention in model systems in vitro, and retained lipoproteins in human plaques are enriched in ceramide, a product of SMase. We now sought to test a direct causative role for acid SMase in lipoprotein retention and atherogenesis in vivo.

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