Heme oxygenase: a target gene for anti-diabetic and obesity.

@article{Abraham2008HemeOA,
  title={Heme oxygenase: a target gene for anti-diabetic and obesity.},
  author={Nader G. Abraham and Peter L. Tsenovoy and John Arthur McClung and George S. Drummond},
  journal={Current pharmaceutical design},
  year={2008},
  volume={14 5},
  pages={
          412-21
        }
}
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 diabetes and obesity. 
Translational Significance of Heme Oxygenase in Obesity and Metabolic Syndrome.
Heme oxygenase in the regulation of vascular biology: from molecular mechanisms to therapeutic opportunities.
TLDR
The rationale for exploring the potential therapeutic role for HO system in the amelioration of vascular inflammation and prevention of adverse cardiovascular outcomes is provided.
Antidiabetic Potential of the Heme Oxygenase-1 Inducer Curcumin Analogues
TLDR
The present review will explore the current understanding of the protective mechanisms of heme oxygenase-1 in diabetes and present some emerging therapeutic options for HO-1 expression in treating diabetic diseases, together with the therapeutic potential of curcumin analogues that have their ability to induce HO- 1 expression.
Heme Oxygenase Upregulation in Obesity and the Metabolic Syndrome.
TLDR
This work has shown that upregulation of HO-1 has had marked beneficial effects on both vascular function and adiposity in animal and human studies and offers a potential long term solution to adiposity by targeting the endothelium.
HO-1 overexpression and underexpression: Clinical implications.
Therapeutic Roles of Heme Oxygenase-1 in Metabolic Diseases: Curcumin and Resveratrol Analogues as Possible Inducers of Heme Oxygenase-1
TLDR
The current understanding of the protective mechanisms of heme oxygenase-1 in metabolic diseases is explored and some emerging therapeutic options for HO-1 expression in treating metabolic diseases are presented, together with the therapeutic potential of curcumin and resveratrol analogues that have their ability to induce HO- 1 expression.
Upregulation of the heme oxygenase system ameliorates postprandial and fasting hyperglycemia in type 2 diabetes.
TLDR
Reducing oxidative stress alongside the concomitant and paradoxical enhancement of insulin secretion and insulin-sensitizing pathways may account for the 3-mo-enduring antidiabetic effect of the heme oxygenase (HO) inducer hemin on Goto-Kakizaki rats, a nonobese insulin-resistant T2D model.
Diabetes Impairs the Vascular Recruitment of Normal Stem Cells by Oxidant Damage, Reversed by Increases in pAMPK, Heme Oxygenase-1, and Adiponectin
Atherosclerosis progression is accelerated in diabetes mellitus (DM) by either direct endothelial damage or reduced availability and function of endothelial progenitor cells (EPCs). Both alterations
HO-1 Upregulation: A Novel Approach in the Treatment of Cardiovascular Disease.
TLDR
Efforts are required to highlight the effects and the ability to target the HO-1 gene in models of obesity with an emphasis on the role of pericardial fat on cardiovascular health.
OX-HDL: A Starring Role in Cardiorenal Syndrome and the Effects of Heme Oxygenase-1 Intervention
TLDR
Findings on how HDL function and the inducible antioxidant gene heme oxygenase-1 (HO-1) are interconnected and how induction of HO-1 is protective against HDL dysfunction and important for the proper functioning of the cardiovascular–renal system are presented.
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TLDR
This work examined whether protection against oxidative stress is altered in patients with diabetes and microangiopathy by examining changes in NADPH oxidase and hemoxygenase‐1 (HO‐1) levels.
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TLDR
3-nitrotyrosine, cellular heme, and superoxide, promoters of vascular damage, are reduced by HO-1 induction, thereby preserving vascular integrity and protecting cardiac function involving an increase in antiapoptotic proteins.
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TLDR
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TLDR
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TLDR
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TLDR
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