Abstract
Heme oxygenase (HO) plays an important role in the cardiovascular system. It is involved in many physiological and pathophysiological processes in all organs of the cardiovascular system. From the regulation of blood pressure and blood flow to the adaptive response to end-organ injury, HO plays a critical role in the ability of the cardiovascular system to respond and adapt to changes in homeostasis. There have been great advances in our understanding of the role of HO in the regulation of blood pressure and target organ injury in the last decade. Results from these studies demonstrate that targeting of the HO system could provide novel therapeutic opportunities for the treatment of several cardiovascular and renal diseases. The goal of this review is to highlight the important role of HO in the regulation of cardiovascular and renal function and protection from disease and to highlight areas in which targeting of the HO system needs to be translated to help benefit patient populations.
Highlights
Heme oxygenase (HO) is the rate-limiting enzyme in the breakdown of heme in the body.Two major isoforms of HO exist: heme oxygenase-1 (HO-1) and heme oxygenase-2 (HO-2)
One mechanism by which induction of HO-1 lowers blood pressure is through decreasing reactive oxygen species (ROS) production which is common in many forms of experimental hypertension [42,43]
This study suggests that short-term induction of HO-1 may chronically lower blood pressure which could be a novel therapeutic approach to circumvent patient compliance issues faced when taking daily anti-hypertensive medications
Summary
Heme oxygenase (HO) is the rate-limiting enzyme in the breakdown of heme in the body. Two major isoforms of HO exist: heme oxygenase-1 (HO-1) and heme oxygenase-2 (HO-2). Both isoforms of HO are expressed in all tissues of the body. Heme oxygenase-2 is the constitutive isoform of HO found in all tissues and cells of the body [2]. Carbon monoxide (CO), the other product derived from HO catabolism of heme, is a gaseous transmitter which can affect ion channels, nitric oxide release, as well as mitochondrial proteins [8,9]. An underappreciated aspect of HO breakdown of heme is the release of free iron and its subsequent sequestration by induction of ferritin. Labile iron is toxic due to its ability to release ROS which can result in cellular damage especially in renal tubule cells [10].
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