scispace - formally typeset
K

Karl A. Nath

Researcher at Mayo Clinic

Publications -  289
Citations -  19298

Karl A. Nath is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Kidney & Heme oxygenase. The author has an hindex of 75, co-authored 254 publications receiving 17628 citations. Previous affiliations of Karl A. Nath include University of Minnesota & Wake Forest University.

Papers
More filters
Journal ArticleDOI

Heme and the vasculature: an oxidative hazard that induces antioxidant defenses in the endothelium

TL;DR: It is shown that heme catalyzes the oxidation of low density lipoproteins which can damage vascular endothelial cells and paradoxically, more prolonged exposure of endothelium to heme or methemoglobin renders them remarkably resistant to oxidant challenge.
Journal ArticleDOI

Control of Oxidative Stress and Inflammation in Sickle Cell Disease with the Nrf2 Activator Dimethyl Fumarate

TL;DR: These studies identify Nrf2 activation as a new therapeutic target for the treatment of SCD as the beneficial effects of DMF were not attributable to decreased hemolysis.
Journal ArticleDOI

The Perfusion Paradox and Vascular Instability in Sickle Cell Disease

TL;DR: The possibility that the induction of heme oxygenase‐1, recently described in SCD, may confer a protective response in the vasculature and other tissues is discussed, and the extent to which alterations in vasoactive systems are involved is explored.
Journal ArticleDOI

Proapoptotic, Antimigratory, Antiproliferative, and Antiangiogenic Effects of Commercial C-Reactive Protein on Various Human Endothelial Cell Types In Vitro: Implications of Contaminating Presence of Sodium Azide in Commercial Preparation

TL;DR: It is concluded that proapoptotic, antiproliferative, antimigratory, and antiangiogenic effects of this commercial CRP preparation on a number of endothelial cell phenotypes in culture may be explained by the presence of sodium azide in this preparation.
Journal ArticleDOI

Renal tubular epithelial cells mimic endothelial cells upon exposure to oxidized LDL.

TL;DR: The cytotoxicity of LDLox on LLC-PK1 cells resembles its toxicity to human umbilical vein endothelial cells (HUVEC) in that oxidized but not native LDL is injurious and it is speculated that LDLox contributes to tubulointerstitial disease in proteinuric states.