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Roles of human liver type fatty acid binding protein in kidney disease clarified using hL‐FABP chromosomal transgenic mice
Author(s) -
KAMIJOIKEMORI ATSUKO,
SUGAYA TAKESHI,
MATSUI KATSUOMI,
YOKOYAMA TAKESHI,
KIMURA KENJIRO
Publication year - 2011
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2011.01469.x
Subject(s) - fatty acid binding protein , pathophysiology , kidney , genetically modified mouse , medicine , transgene , kidney disease , disease , biomarker , renal function , urinary system , in vivo , pathology , endocrinology , gene , biology , biochemistry , genetics
Kidney disease develops to renal failure over a period of days, months or years, hence, clinical markers that indicate the real‐time renal pathophysiological conditions is important. Liver type fatty acid binding protein (L‐FABP) is a 14 kDa molecule predominantly expressed in human proximal tubules. Clinical studies demonstrate that urinary excretion of L‐FABP derived from the proximal tubules is an excellent biomarker for predicting and monitoring deterioration of renal function or for early detection of kidney disease. However, in order to clarify the pathophysiological roles or dynamics of renal L‐FABP in diseased settings, in vivo experimental studies of kidney diseases are indispensable. Since L‐FABP is not endogenously expressed in murine kidneys, a transgenic (Tg) mouse model with expression of the human L‐FABP gene was established. This review article summarizes the findings on the pathophysiological roles and dynamics of renal human L‐FABP in the recent experimental studies performed using this Tg mouse model.