Heme oxygenase, a novel target for the treatment of hypertension and obesity?

Peter Hosick, David E. Stec

Research output: Contribution to journalReview articleResearchpeer-review

28 Citations (Scopus)

Abstract

Heme oxygenase (HO) is the rate-limiting enzyme in the metabolism of heme-releasing bioactive molecules carbon monoxide (CO), biliverdin, and iron, each with beneficial cardiovascular actions. Biliverdin is rapidly reduced to bilirubin, a potent antioxidant, by the enzyme biliverdin reductase, and iron is rapidly sequestered by ferritin in the cell. Several studies have demonstrated that HO-1 induction can attenuate the development of hypertension as well as lower blood pressure in established hypertension in both genetic and experimental models. HO-1 induction can also reduce target organ injury and can be beneficial in cardiovascular diseases, such as heart attack and stroke. Recent studies have also identified a beneficial role for HO-1 in the regulation of body weight and metabolism in diabetes and obesity. Chronic HO-1 induction lowers body weight and corrects hyperglycemia and hyperinsulinemia. Chronic HO-1 induction also modifies the phenotype of adipocytes in obesity from one of large, cytokine producing to smaller, adiponectin producing. Finally, chronic induction of HO-1 increases oxygen consumption, CO 2 , and heat production and activity in obese mice. This review will discuss the current understanding of the actions of the HO system to lower blood pressure and body weight and how HO or its metabolites may be ideal candidates for the development of drugs that can both reduce blood pressure and lower body weight.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume302
Issue number2
DOIs
StatePublished - 1 Jan 2012

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Heme Oxygenase (Decyclizing)
Heme Oxygenase-1
Obesity
Hypertension
Body Weight
Biliverdine
biliverdin reductase
Carbon Monoxide
Blood Pressure
Iron
Obese Mice
Thermogenesis
Genetic Models
Adiponectin
Hyperinsulinism
Enzymes
Ferritins
Heme
Bilirubin
Adipocytes

Keywords

  • Adiponectin
  • Bilirubin
  • Biliverdin
  • Carbon monoxide
  • Inflammation
  • Kidney

Cite this

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title = "Heme oxygenase, a novel target for the treatment of hypertension and obesity?",
abstract = "Heme oxygenase (HO) is the rate-limiting enzyme in the metabolism of heme-releasing bioactive molecules carbon monoxide (CO), biliverdin, and iron, each with beneficial cardiovascular actions. Biliverdin is rapidly reduced to bilirubin, a potent antioxidant, by the enzyme biliverdin reductase, and iron is rapidly sequestered by ferritin in the cell. Several studies have demonstrated that HO-1 induction can attenuate the development of hypertension as well as lower blood pressure in established hypertension in both genetic and experimental models. HO-1 induction can also reduce target organ injury and can be beneficial in cardiovascular diseases, such as heart attack and stroke. Recent studies have also identified a beneficial role for HO-1 in the regulation of body weight and metabolism in diabetes and obesity. Chronic HO-1 induction lowers body weight and corrects hyperglycemia and hyperinsulinemia. Chronic HO-1 induction also modifies the phenotype of adipocytes in obesity from one of large, cytokine producing to smaller, adiponectin producing. Finally, chronic induction of HO-1 increases oxygen consumption, CO 2 , and heat production and activity in obese mice. This review will discuss the current understanding of the actions of the HO system to lower blood pressure and body weight and how HO or its metabolites may be ideal candidates for the development of drugs that can both reduce blood pressure and lower body weight.",
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Heme oxygenase, a novel target for the treatment of hypertension and obesity? / Hosick, Peter; Stec, David E.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 302, No. 2, 01.01.2012.

Research output: Contribution to journalReview articleResearchpeer-review

TY - JOUR

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AU - Stec, David E.

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