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miR-21 is a key therapeutic target for renal injury in a mouse model of type 2 diabetes
Aims/hypothesisAs microRNA-21 (miR-21) plays a pathological role in fibrosis, we hypothesised that it may be a therapeutic target for diabetic nephropathy.MethodsAbundance of miR-21 was examined inExpand
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Angiotensin II up-regulates angiotensin I-converting enzyme (ACE), but down-regulates ACE2 via the AT1-ERK/p38 MAP kinase pathway.
The recent discovery of the angiotensin II (Ang II)-breakdown enzyme, angiotensin I converting enzyme (ACE) 2, suggests the importance of Ang II degradation in hypertension. The present studyExpand
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Angiotensin II Induces Connective Tissue Growth Factor and Collagen I Expression via Transforming Growth Factor–&bgr;–Dependent and –Independent Smad Pathways: The Role of Smad3
Connective tissue growth factor (CTGF) plays a critical role in angiotensin II (Ang II)–mediated hypertensive nephropathy. The present study investigated the mechanisms and specific roles ofExpand
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miR-192 mediates TGF-beta/Smad3-driven renal fibrosis.
TGF-beta/Smad3 promotes renal fibrosis, but the mechanisms that regulate profibrotic genes remain unclear. We hypothesized that miR-192, a microRNA expressed in the kidney may mediate renal fibrosisExpand
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Chemokines in renal injury.
  • A. C. Chung, H. Lan
  • Medicine
  • Journal of the American Society of Nephrology…
  • 1 May 2011
The main function of chemokines is to guide inflammatory cells in their migration to sites of inflammation. During the last 2 decades, an expanding number of chemokines and their receptors haveExpand
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The Protective Role of Smad7 in Diabetic Kidney Disease: Mechanism and Therapeutic Potential
OBJECTIVE Although Smad3 has been considered as a downstream mediator of transforming growth factor-β (TGF-β) signaling in diabetes complications, the role of Smad7 in diabetes remains largelyExpand
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Smad7 suppresses renal fibrosis via altering expression of TGF-β/Smad3-regulated microRNAs.
Blockade of transforming growth factor-β (TGF-β) signaling by Smad7 gene therapy is known to prevent experimental renal fibrosis. This study investigated whether Smad7 suppresses renal fibrosis viaExpand
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Identification of novel long noncoding RNAs associated with TGF-β/Smad3-mediated renal inflammation and fibrosis by RNA sequencing.
We have previously shown that transforming growth factor-β/Smad3-dependent miRNAs play a critical role in renal inflammation and fibrosis. However, off-target effects of miRNAs limit theirExpand
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Advanced glycation end-products induce tubular CTGF via TGF-beta-independent Smad3 signaling.
Advanced glycation end-products (AGEs) can induce expression of connective tissue growth factor (CTGF), which seems to promote the development of diabetic nephropathy, but the exact signalingExpand
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Disruption of the Smad7 gene promotes renal fibrosis and inflammation in unilateral ureteral obstruction (UUO) in mice.
BACKGROUND The present study tested the hypothesis that disruption of Smad7 function may accelerate renal fibrosis and inflammation. METHODS This was investigated in a unilateral ureteralExpand
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