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Raghu Kalluri

Researcher at University of Texas MD Anderson Cancer Center

Publications -  325
Citations -  89851

Raghu Kalluri is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Cancer & Angiogenesis. The author has an hindex of 115, co-authored 306 publications receiving 71127 citations. Previous affiliations of Raghu Kalluri include Beth Israel Deaconess Medical Center & Baylor College of Medicine.

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Starting the scar: A primary role for pericytes?

TL;DR: The authors tracked a population of pericytes, type A pericytic cells, in a mouse model of spinal cord injury and found that descendants of these pericycletes were required for scar formation.
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Specific activation of K-RasG12D allele in the bladder urothelium results in lung alveolar and vascular defects.

TL;DR: It is suggested that altered protease activity in amniotic fluid might be associated with matrix defects in lung of UPK II-Cre;LSL-K-rasG12 and these defects resemble those observed in early stage human neonatal bronchopulmonary dysplasia (BPD), although the relevance of this new mouse model for BPD study needs further investigation.
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An unusual case of pulmonary-renal syndrome associated with defects in type IV collagen composition and anti-glomerular basement membrane autoantibodies

TL;DR: These findings represent the first known case of human autoantibodies to the alpha2NC1 domain and show that this patient has decreased alpha3 and alpha5 chain expression in the GBM and defects in type IV collagen, resembling abnormalities in patients with Alport's syndrome.
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Stem cell-based therapy for glomerular diseases: an evolving concept.

TL;DR: Alport syndrome is a genetic disease that affects kidneys, ears, and eyes as a result of mutations in basement membrane collagen genes COL4A3,COL4A4, and COL4 a5, encoding the α3, α4,and α5 chains of type IV collagen chains.
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Circulating endoglin concentration is not elevated in chronic kidney disease.

TL;DR: Renal function is not associated with the circulating concentration of soluble endoglin, and Elevations in solubleendoglin concentration are unlikely to contribute to the progression of CKD or the predisposition of individuals with CKD to develop cardiovascular disease.