| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2081949 | Drug Discovery Today: Disease Mechanisms | 2007 | 6 Pages |
Heme oxygenase (HO) has been shown to be critical for attenuating reactive oxygen species (ROS) through its ability to degrade heme and produce carbon monoxide (CO) and bilirubin. Excess free heme and proinflammatory growth factors are major contributors to acute kidney injury (AKI). Site-specific delivery of HO-1 to renal structures, that is, to the medullary thick ascending limb of the loop of heme (mTALH), has been shown to normalize blood pressure and provide protection against oxidative injury. Diabetes-mediated renal dysfunction in HO-2 deficiency may well be related to a tissue environment undergoing oxidative stress in the absence of HO-derived bilirubin and CO. Induction of HO-1 decreases superoxide, maintain normal plasma creatinine levels and prevent renal tubular and microvascular damage in HO-2-deficient mice. This review will demonstrate that the HO system is vital for the preservation of renal structural and functional integrity.
Section editor:Michael S. Goligorsky – Renal Research Institute, New York Medical College, Valhalla, NY, USA
