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2018 ; 37
(1
): 30-40
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Human CD36 overexpression in renal tubules accelerates the progression of renal
diseases in a mouse model of folic acid-induced acute kidney injury
#MMPMID29629275
Jung JH
; Choi JE
; Song JH
; Ahn SH
Kidney Res Clin Pract
2018[Mar]; 37
(1
): 30-40
PMID29629275
show ga
BACKGROUND: Acute kidney injury (AKI) is a risk factor for progression to chronic
kidney disease, with even subclinical AKI episodes progressing to chronic kidney
disease. Several risk factors such as preexisting kidney disease, hyperglycemia,
and hypertension may aggravate renal disease after AKI. However, mechanisms
underlying the progression of AKI are still unclear. This study identified the
effect of human cluster of differentiation 36 (CD36) overexpression on the
progression of folic acid-induced AKI. METHODS: Pax8-rtTA/tetracycline response
element-human CD36 transgenic mice were used to elucidate the effect of human
CD36 overexpression in the proximal tubules on folic acid-induced AKI. RESULTS:
Results of histological analysis showed severely dilated tubules with casts and
albuminuria in folic acid-treated transgenic mice overexpressing human CD36
compared with folic acid-treated wild-type mice. In addition, analysis of mRNA
expression showed a significant increase in the collagen 3a1 gene in folic
acid-treated transgenic mice overexpressing human CD 36 compared with folic
acid-treated wild type mice. CONCLUSION: Human CD36-overexpressing transgenic
mice showed severe pathological changes and albuminuria compared with wild-type
mice. Moreover, mRNA expression of the collagen 3a1 gene increased in folic
acid-treated transgenic mice. These results suggest that human CD36
overexpression is a risk factor of AKI and its progression to chronic kidney
disease.