Hypertrophic cardiomyopathy with type I CD36 deficiency

被引：11

作者：

Watanabe, K

Toba, K

Ogawa, Y

Kodama, M

Hirono, S

Ohkura, Y

Hanawa, H

Nakamura, Y

Aoki, Y

Fuse, I

Aizawa, Y

Miyajima, S

Kusano, Y

Nagatomo, T

Hasegawa, G

Naito, M

机构：

[1] Niigata Coll Pharm, Niigata 9502081, Japan

[2] Niigata Univ, Sch Med, Dept Med 1, Niigata, Japan

[3] Niigata Univ, Sch Med, Dept Pathol 2, Niigata, Japan

[4] Tsubame Rousai Hosp, Div Cardiol, Niigata, Japan

来源：

JAPANESE CIRCULATION JOURNAL-ENGLISH EDITION | 1998年 / 62卷 / 07期

关键词：

CD36; deficiency; endothelial cell; hypertrophic cardiomyopathy; I-123-BMIPP; long-chain fatty acid;

D O I：

10.1253/jcj.62.541

中图分类号：

N09 [自然科学史]; B [哲学、宗教];

学科分类号：

01 ; 0101 ; 010108 ; 060207 ; 060305 ; 0712 ;

摘要：

CD36 is a multifunctional membrane-type receptor glycoprotein that reacts with oxidized low-density lipoprotein and long-chain fatty acid (LCFA). A patient presented with hereditary hypertrophic cardiomyopathy (HCM) and type I CD36 deficiency (neither platelets nor monocytes expressed CD36) but showed no myocardial LCFA accumulation. CD36 was expressed in the capillary endothelial cells of the cardiac muscle of a control subject, while the patient's myocardial capillary endothelial cells were completely CD36-negative. These results suggest that type I CD36 deficiency is closely related to hereditary HCM and lack of myocardial LCFA accumulation.

引用

页码：541 / 542

页数：2

共 7 条

[1]

ABUMRAD NA, 1993, J BIOL CHEM, V268, P17665

[2] HEART CD36 EXPRESSION IS INCREASED IN MURINE MODELS OF DIABETES AND IN MICE FED A HIGH-FAT DIET [J].