Current Pharmaceutical Design - Volume 14, Issue 5, 2008

In 2003, the issue of Current Pharmaceutical Design entitled “Modulation of heme oxygenase-1 as a therapeutic target” presented six papers focused on the role and interest of heme oxygenase(HO)-1 modulation in human disease. This topic has generated significant interest in the last years leading to a growing number of publications. The purpose of this issue of Current Pharmaceutical Design is to highlight studies exa Read More

Heme oxygenase-1 (HO-1) is central to the regulation of oxidative injury. The role of increased HO-1 expression and Heme oxygenase (HO) activity in mitigating the detrimental side effect of diabetes is examined. A review of the mechanism(s) of action is included. This may lead to the development of pharmacological and genetic approaches to mitigate the clinical complications associated with the progression of diabet Read More

Great attention has been placed on the protective role of heme oxygenase-1 (HO-1) for several vascular diseases such as atherosclerosis. HO-1, by exerting anti-inflammatory, antiproliferative, anti-apoptotic and anti-oxidant effects on the vasculature, protects against atherosclerosis. The precise underlying mechanisms for HO-1-based protection are not yet completely understood, but appear to involve the protective effec Read More

Heme oxygenase-1 (HO-1) catalyzes the degradation of heme to generate carbon monoxide, biliverdin and free iron. Increased HO-1 levels constitute an anatomopathological feature of many neurological diseases, such as neurodegenerative disorders and brain infections, which correlate with exacerbated oxidative stress and inflammation. It is generally accepted that the elevated HO-1 levels represent an attem Read More

The constitutive isoform of heme oxygenase, HO-2, is highly expressed in the brain and in cerebral vessels. HO-2 functions in the brain have been evaluated using pharmacological inhibitors of the enzyme and HO-2 gene deletion in in vivo animal models and in cultured cells (neurons, astrocytes, cerebral vascular endothelial cells). Rapid activation of HO-2 via post-translational modifications without upregulation of HO- Read More

Heme oxygenase-1 (HO-1) is the rate-limiting enzyme of ferroheme metabolic pathway, which has the functions of antioxidation, anti-inflammatory, anti-apoptosis and anti-smooth muscle hyperplasia. Furthermore, HO-1 exerts a protective action in the diseases mediated by effector T lymphocytes such as T helper (Th) 1, Th2 and Th17. In addition, regulatory T cells (Treg) control the activity of CD4+CD25- eff Read More

Carbon monoxide (CO) mediates many of the biological effects that are attributed to heme oxygenase (HO), the enzyme responsible for CO production in mammals. Antioxidant and anti-inflammatory activities of HO-1, the inducible isoform of heme oxygenase, have been demonstrated in a variety of disease models and a therapeutic exploitation of this pathway is currently under scrutiny. In this context, the liberation of Read More

Heme oxygenase-1 (HO-1) is an inducible rate-limiting enzyme which catalyzes group heme into carbon monoxide, iron and bilirubin. In the recent years, HO-1 expression has been reported as an important protective endogenous mechanism against physical, chemical and biological stress. In this regard, induction of this enzyme has shown beneficial effects in several pathologic conditions, such as inflammatory processes, athe Read More

Diabetic vascular complication is a leading cause of acquired blindness, end-stage renal failure, a variety of neuropathies and accelerated atherosclerosis, which could account for disabilities and high mortality rates in patients with diabetes. Although several hyperglycemia- elicited metabolic and hemodynamic derangements have been implicated in the pathogenesis of diabetic vascular complication, the process of Read More

Liver ischemia-reperfusion injury occurs in a number of clinical settings, including liver surgery, transplantation, and circulatory shock, leading to significant morbidity and mortality. There is a substantial evidence that hepatic ischemia-reperfusion injury results from an intense inflammatory response initiated by oxidative stress in the liver parenchyma during reperfusion. The anti-inflammatory effects of glucocorticosteroids ( Read More