TY - JOUR
T1 - Etiological significance of apolipoprotein E mutations in lipoprotein glomerulopathy
AU - Saito, Takao
AU - Ishigaki, Yasushi
AU - Oikawa, Shinichi
AU - Yamamoto, Tokuo T.
N1 - Funding Information:
This work was supported by grants for the Specific Renal Disease Research Projects from the Ministry of Health, Labor and Welfare, Japan, and a grant-in-aid (#10670982) from the Ministry of Education Science and Culture. We thank Dr. Ian Gleadall for review of the manuscript and Shizue Mochizuki for technical assistance.
PY - 2002
Y1 - 2002
N2 - Lipoprotein glomerulopathy (LPG) is a newly recognized renal disease characterized by thrombus-like lipoproteins in the glomerular capillaries and abnormal lipoprotein profiles similar to those in type III hyperlipoproteinemia. Recently, these conditions have been shown to be associated with some apolipoprotein E (apoE) mutations. We found an apoE mutation (designated apoE-Sendai) that substitutes arginine 145 with proline. This mutation occurs most frequently in Japanese patients with LPG. To elucidate the etiological role of this mutation in the apoE gene, we established an experimental model for LPG by transducing apoE-Sendai in apoE knockout mice with the use of an adenovirus vector. Based on the findings in patients with LPG and its animal model, we suggest that the glomerular lesions are not only caused by hyperlipidemia, but also by in situ interaction between lipoprotein-containing mutant apoE with the glomerulus. In this review, we outline the clinical features of LPG and discuss the relationship between apoE mutations and LPG.
AB - Lipoprotein glomerulopathy (LPG) is a newly recognized renal disease characterized by thrombus-like lipoproteins in the glomerular capillaries and abnormal lipoprotein profiles similar to those in type III hyperlipoproteinemia. Recently, these conditions have been shown to be associated with some apolipoprotein E (apoE) mutations. We found an apoE mutation (designated apoE-Sendai) that substitutes arginine 145 with proline. This mutation occurs most frequently in Japanese patients with LPG. To elucidate the etiological role of this mutation in the apoE gene, we established an experimental model for LPG by transducing apoE-Sendai in apoE knockout mice with the use of an adenovirus vector. Based on the findings in patients with LPG and its animal model, we suggest that the glomerular lesions are not only caused by hyperlipidemia, but also by in situ interaction between lipoprotein-containing mutant apoE with the glomerulus. In this review, we outline the clinical features of LPG and discuss the relationship between apoE mutations and LPG.
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U2 - 10.1016/S1050-1738(01)00148-7
DO - 10.1016/S1050-1738(01)00148-7
M3 - Review article
C2 - 11852253
AN - SCOPUS:0036170002
VL - 12
SP - 67
EP - 70
JO - Trends in Cardiovascular Medicine
JF - Trends in Cardiovascular Medicine
SN - 1050-1738
IS - 2
ER -