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Journal ArticleDOI

Carbon monoxide from heme catabolism protects against hepatobiliary dysfunction in endotoxin-treated rat liver.

TLDR
Protective roles of CO against hepatobiliary dysfunction caused by heme overloading under stress conditions are suggested.
About
This article is published in Gastroenterology.The article was published on 2001-04-01. It has received 161 citations till now. The article focuses on the topics: Heme oxygenase & Heme.

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Citations
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Journal ArticleDOI

Heme oxygenase-1: the "emerging molecule" has arrived.

TL;DR: This review highlights current information on the function of HO-1 and its relevance to specific pulmonary and cardiovascular diseases and shows its anti-inflammatory, antiapoptotic, and antiproliferative effects.
Journal ArticleDOI

The hepatic microcirculation: mechanistic contributions and therapeutic targets in liver injury and repair

TL;DR: The use of the recently introduced techniques to monitor the hepatic microcirculation in humans, such as near-infrared spectroscopy or orthogonal polarized spectral imaging, may allow an early initiation of treatment, which should benefit the final outcome of these critically ill patients.
Journal ArticleDOI

Heme is a potent inducer of inflammation in mice and is counteracted by heme oxygenase.

TL;DR: It is demonstrated for the first time that heme induces increased vascular permeability, adhesion molecule expression, and leukocyte recruitment in vivo, whereas HO antagonizes heme-induced inflammation possibly through the down-modulation of adhesion molecules.
Journal ArticleDOI

Heme oxygenase-1: redox regulation and role in the hepatic response to oxidative stress.

TL;DR: Evidence suggests that protective effects of up-regulation of the HO pathway--presumably through production of bile pigments and CO--have been reported for a variety of cells and tissues, including the liver, evidence suggests that the protective action might be restricted to a rather narrow threshold of overexpression.
Journal ArticleDOI

Interactions of multiple gas-transducing systems: hallmarks and uncertainties of CO, NO, and H2S gas biology.

TL;DR: This work takes an integrated approach to the interaction of gases by considering the physiological significance of CO, NO, CO, and H2S on mitochondrial cytochrome c oxidase, a key target and central mediator of mitochondrial respiration.
References
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Journal ArticleDOI

A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group.

TL;DR: A restrictive strategy of red-cell transfusion is at least as effective as and possibly superior to a liberal transfusion strategy in critically ill patients, with the possible exception of patients with acute myocardial infarction and unstable angina.
Journal ArticleDOI

Heme oxygenase: function, multiplicity, regulatory mechanisms, and clinical applications.

TL;DR: In this review recent findings on heme oxygenase are highlighted and it is shown that the enzyme activity is inhibited in vivo for extended periods subsequent to binding of Zn- and Sn- protoporphyrins.
Journal ArticleDOI

Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency

TL;DR: The first known human case of heme oxygenase-1 (HO-1) deficiency is presented and clues to the key roles played by this important enzyme in vivo are provided.
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Heme oxygenase-1: function, regulation, and implication of a novel stress-inducible protein in oxidant-induced lung injury.

TL;DR: The magnitude ofHO-1 induction after oxidative stress and the wide distribution of this enzyme in systemic tissues coupled with the intriguing biological activities of the catalytic byproducts, carbon monoxide, iron, and bilirubin makes HO-1 a highly attractive and interesting candidate stress-response protein which may play key role(s) in mediating protection against oxidant-mediated lung injury.
Journal ArticleDOI

Heme oxygenase 1 is required for mammalian iron reutilization

TL;DR: Results indicate that Hmox1 has an important recycling role by facilitating the release of iron from hepatic and renal cells, and describe a mouse model of human iron metabolic disorders.
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