Kidney injury molecule-1 (KIM-1) mediates renal epithelial cell repair via ERK MAPK signaling pathway

نویسندگان
چکیده

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

IGF-1 protects tubular epithelial cells during injury via activation of ERK/MAPK signaling pathway

Injury of renal tubular epithelial cells can induce acute renal failure and obstructive nephropathy. Previous studies have shown that administration of insulin-like growth factor-1 (IGF-1) ameliorates the renal injury in a mouse unilateral ureteral obstruction (UUO) model, whereas the underlying mechanisms are not completely understood. Here, we addressed this question. We found that the admini...

متن کامل

Kidney injury molecule-1 (KIM-1): a novel kidney-specific injury molecule playing potential double-edged functions in kidney injury.

Kidney injury molecule-1 (KIM-1), a recently discovered transmembrane protein, is expressed in dedifferentiated proximal renal tubular epithelial cells in damaged regions. It may participate in the progress of renal injury or repair. Many studies have illustrated the different functions of KIM-1 in various renal diseases including protective functions in acute kidney injury and damaging functio...

متن کامل

Kidney Injury Molecule-1 is Elevated in Nephropathy and Mediates Macrophage Activation via the Mapk Signalling Pathway.

BACKGROUND/AIMS Kidney injury molecule-1 (KIM-1) is highly expressed in renal tubular cells after injury and is usually regarded as an early biomarker of acute kidney injury(AKI). The aim of this study was to determine the role of KIM-1 in the development of renal tubular injury Methods: Clinical samples, three different animal models and in vitro experiments were utilized to determine the poss...

متن کامل

Kidney Injury Molecule-1 (Kim-1) expression in murine polycystic kidney disease

Kidney Injury Molecule-1 (Kim-1) is a type 1 membrane protein maximally upregulated in proliferating and de-differentiated tubular cells after renal ischemia. Since epithelial dedifferentiation, proliferation and local ischemia may play a role in the pathophysiology of autosomal dominant polycystic kidney disease (ADPKD), we investigated Kim-1 expression in a mouse model of this disease. In the...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Molecular and Cellular Biochemistry

سال: 2016

ISSN: 0300-8177,1573-4919

DOI: 10.1007/s11010-016-2700-7