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Takashi Wada

Researcher at Kanazawa University

Publications -  450
Citations -  12779

Takashi Wada is an academic researcher from Kanazawa University. The author has contributed to research in topics: Kidney disease & Kidney. The author has an hindex of 52, co-authored 404 publications receiving 10475 citations. Previous affiliations of Takashi Wada include University of Tokyo & Jikei University School of Medicine.

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Essential involvement of interleukin-8 (IL-8) in acute inflammation.

TL;DR: A highly specific neutralizing antibody against IL‐8 was administered in several types of acute inflammatory reactions, including lipopolysaccharide‐induced dermatitis, LPS/IL‐1‐induced arthritis, lung reperfusion injury, and acute immune complex‐type glomerulonephritis to suggest thatIL‐8 plays a causative role in acute inflammation by recruiting and activating neutrophils.
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Up-regulation of monocyte chemoattractant protein-1 in tubulointerstitial lesions of human diabetic nephropathy

TL;DR: Observations suggest that locally produced MCP-1 may be involved in the development of advanced diabetic nephropathy, especially in the formation of tubulointerstitial lesions possibly through Mphi recruitment and activation.
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Blockade of CCR2 ameliorates progressive fibrosis in kidney.

TL;DR: In this paper, the authors investigated renal interstitial fibrosis induced by a unilateral ureteral obstruction in CCR2 gene-targeted mice and mice treated with propagermanium or RS-504393, cCR2 inhibitors.
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ADAMTS-1: a metalloproteinase-disintegrin essential for normal growth, fertility, and organ morphology and function.

TL;DR: ADAMTS-1 thus appears necessary for normal growth, fertility, and organ morphology and function, and the resemblance of the renal phenotype to human ureteropelvic junction obstruction may provide a clue to the pathogenesis of this common congenital disease.
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Secondary lymphoid tissue chemokine (SLC/CCL21)/CCR7 signaling regulates fibrocytes in renal fibrosis.

TL;DR: It is suggested that CCR7-positive fibrocytes infiltrate the kidney via CCL21-positive vessels, thereby contributing to the pathogenesis of renal fibrosis.