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Effect of AT
2
receptor blockade on the pathogenesis of renal fibrosis
Jeremiah J. Morrissey
, Saulo Klahr
Section of Clinical and Translational Research
Institute of Clinical and Translational Sciences (ICTS)
Siteman Cancer Center
COVID-19 Researchers
Institute for Public Health
Research output
:
Contribution to journal
›
Article
›
peer-review
120
Scopus citations
Overview
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2
receptor blockade on the pathogenesis of renal fibrosis'. Together they form a unique fingerprint.
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Keyphrases
Receptor Blockade
100%
Kidney
100%
Renal Fibrosis
100%
AT2 Receptor
100%
Angiotensin II (Ang II)
60%
Ureter
60%
Obstructed Kidney
60%
Receptor Antagonist
40%
Angiotensin II Type 1 Receptor (AT1R)
40%
Obstructive Nephropathy
40%
PD123319
40%
Apoptosis
20%
Fibrosis
20%
P53 Expression
20%
Antifibrotic
20%
Cellular Events
20%
Receptor Antagonism
20%
Molecular Events
20%
α-smooth muscle Actin (α-SMA)
20%
Monocyte-derived Macrophages
20%
Unilateral Ureteral Obstruction
20%
Interstitial Collagens
20%
Angiotensin-converting Enzyme Inhibition
20%
Tubular Cells
20%
Interstitium
20%
Tubulointerstitial Fibrosis
20%
Macrophage Infiltration
20%
Profibrotic
20%
Collagen IV
20%
Interstitial Volume
20%
Medicine and Dentistry
Receptor
100%
Angiotensin II
100%
Receptor Blocking
100%
Kidney Fibrosis
100%
Fibrosis
66%
Nephropathy
66%
Angiotensin 2 Receptor Antagonist
66%
Macrophage
33%
Protein P53
33%
Ureter
33%
Programmed Cell Death
33%
Dipeptidyl Carboxypeptidase
33%
Obstruction
33%
Ureter Obstruction
33%
Smooth Muscle Actin
33%
Interstitium
33%
Enzyme Inhibition
33%
Pharmacology, Toxicology and Pharmaceutical Science
Receptor
100%
Kidney Fibrosis
100%
Angiotensin II
75%
Fibrosis
50%
Kidney Disease
50%
Angiotensin 2 Receptor Antagonist
50%
Dipeptidyl Carboxypeptidase
25%
Obstruction
25%
Smooth Muscle Actin
25%
Protein P53
25%
Enzyme Inhibition
25%
Ureter Obstruction
25%