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Editorial
. 2017 Aug;28(8):2253-2255.
doi: 10.1681/ASN.2017030320. Epub 2017 Apr 25.

Endothelin-A Receptor Antagonism Retards the Progression of Murine Sickle Cell Nephropathy

Karl A Nath  1 , Zvonimir S Katusic  2   3
Affiliations
Editorial

Endothelin-A Receptor Antagonism Retards the Progression of Murine Sickle Cell Nephropathy

Karl A Nath et al. J Am Soc Nephrol. 2017 Aug.
No abstract available

Keywords: endothelin; heme; hemoglobin S; hemolysis; kidney; sickle cell disease.

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Figures

Figure 1:
Figure 1:
Positive feedback loop involving endothelin-1 (ET-1) and hemolysis in sickle cell nephropathy. In sickle cell disease vasoocclusion predisposes to hemolysis and the release of sickle hemoglobin (HbS) into plasma. HbS binds nitric oxide (NO), and such loss of NO from the vasculature increases the synthesis of ET-1. HbS undergoes autooxidation leading to the generation of reactive oxygen species (ROS), HbS denaturation, and the liberation of heme. Heme, through the generation of ROS and induction of placenta growth factor (PlGF), induces cellular synthesis of ET-1. By engaging the endothelin-A (ETA) receptor, ET-1 causes vasoconstriction, generates ROS, and induces inflammation, all of which may provide a positive feedback loop that sustains this hemolysis-dependent cycle.
See this image and copyright information in PMC

Comment on

References

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