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Anthony J. Croatt

Researcher at Mayo Clinic

Publications -  73
Citations -  5461

Anthony J. Croatt is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Kidney & Heme oxygenase. The author has an hindex of 40, co-authored 70 publications receiving 5128 citations. Previous affiliations of Anthony J. Croatt include University of Minnesota & Ochsner Health System.

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Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemia-reperfusion injury.

TL;DR: In vivo depletion of DCs from the kidney substantially attenuated TNF secretion by total and CD45(+ve) cells following IRI, uncovering a role for resident F4/80( +ve) DCs as the predominant secretors of TNF within 24 h of IRI.

Resident dendritic cells are the predominant TNF-secreting cell in early renal ischemia-reperfusion

TL;DR: In this paper, the contribution of dendritic cells (DCs) to early production of TNF and other inflammatory mediators was investigated in renal ischemia-reperfusion injury (IRI) patients.
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The indispensability of heme oxygenase-1 in protecting against acute heme protein-induced toxicity in vivo.

TL;DR: The induction of HO-1 is an indispensable response in protecting against acute heme protein toxicity in vivo, and doses of hemoglobin precipitate rapidly developing, acute renal failure and marked mortality inHO-1 -/- mice.
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Induction of heme oxygenase in toxic renal injury: A protective role in cisplatin nephrotoxicity in the rat

TL;DR: It is confirmed that tin protoporphyrin prevented the increase in heme oxygenase activity induced by cisplatin, which was associated with increased kidney heme content and ferritin content.
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Heme protein-induced chronic renal inflammation: suppressive effect of induced heme oxygenase-1.

TL;DR: It is concluded that up-regulation of HO-1 occurs in the kidney in humans and rats repetitively exposed to heme proteins, which represents an anti-inflammatory response since the genetic deficiency ofHO-1 markedly increases activation of NF-kappaB, MCP-1 expression, and tubulointerstitial cellular inflammation.