Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

Ahlström, Katarina; Biber, Björn; Åberg, Anna-Maja; Waldenström, Anders; Ronquist, Gunnar; Abrahamsson, Pernilla; Strandén, Per; Johansson, Gillis; Haney, Michael

doi:10.1111/j.1399-6576.2009.01992.x

Cited by 16 publications

(9 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The improvement of oxidative metabolism by restoring high energy stores (in particular ATP) without any glycolysis stimulation appears to confer neuroprotection in a cerebral preconditioning model (35). In myocardium ischemia, CO reduced glycolytic metabolism response (36). Furthermore, in macrophages, CO activated hypoxia-inducing factor-1 without increasing the rate of glycolysis (33).…”

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide Modulates Apoptosis by Reinforcing Oxidative Metabolism in Astrocytes

Almeida

Queiroga

Sousa

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Low doses of carbon monoxide (CO) prevent apoptosis in several cell models, including astrocytes. Results: CO improves cytochrome c oxidase (COX) activity and induces mitochondrial biogenesis. Bcl-2 expression and interaction with COX is involved in CO signaling. Conclusion: CO stimulates oxidative phosphorylation, improves metabolism, and prevents astrocytic apoptosis. Significance: Metabolism modulation can be a potential strategy against cerebral ischemia.

show abstract

Section: Discussionmentioning

confidence: 99%

Carbon Monoxide Modulates Apoptosis by Reinforcing Oxidative Metabolism in Astrocytes

Almeida

Queiroga

Sousa

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…171 Similarly, pigs exposed to CO gas inhalation for 3 h (5% HbCO) and subsequently subjected to coronary occlusion showed a much lower concentration of lactate in blood, less utilization of glucose and increased pyruvate levels during ischemia compared to untreated animals, while cardiac ATP and energy charge were unchanged between the two groups. 172 It is known that pyruvate dehydrogenase is inhibited in the heart by increased fatty acid β-oxidation 173 and it is tempting to suggest that reduced lactate in association with increased pyruvate are due to a CO-mediated switch in substrate utilization for energy. Altogether, these findings indicate that the HO-1/CO pathway exerts some of its cardiac protective effects by dynamically regulating aerobic and anabolic metabolisms and thus counteracting the metabolic dysfunction occurring during stress conditions.…”

Section: Interaction Of Co With Cellular Targetsmentioning

confidence: 99%

Heme Oxygenase-1 and Carbon Monoxide in the Heart

Otterbein

Foresti

Motterlini

2016

Circulation Research

178

View full text Add to dashboard Cite

Understanding the processes governing the ability of the heart to repair and regenerate after injury is crucial for developing translational medical solutions. New avenues of exploration include cardiac cell therapy and cellular reprogramming targeting cell death and regeneration. An attractive possibility is the exploitation of cytoprotective genes that exist solely for self-preservation processes and serve to promote and support cell survival. While the antioxidant and heat shock proteins are included in this category, one enzyme that has received a great deal of attention as a master protective sentinel is heme oxygenase-1 (HO-1), the rate-limiting step in the catabolism of heme into the bioactive signaling molecules carbon monoxide, biliverdin and iron. The remarkable cardioprotective effects ascribed to HO-1 are best evidenced by its ability to regulate inflammatory processes, cellular signaling and mitochondrial function ultimately mitigating myocardial tissue injury and the progression of vascular-proliferative disease. We discuss here new insights into the role of HO-1 and heme on cardiovascular health, and importantly, how they might be leveraged to promote heart repair after injury.

show abstract

“…Likewise, in a similar model of heart ischemia in pigs, CO was administrated at concentrations with the goal to obtain up to 5% of carboxyhaemglobin in the blood. In CO-treated animals the lactate production/glucose consumption ratio decreased, meaning that higher amounts of pyruvate entered and were metabolized by TCA cycle and a decrease on glycolytic metabolism was observed [37]. In human hepatocytes or primary culture of mouse hepatocytes, exogenous or heam-oxygenase-1-derived CO stimulated ATP generation [38, 39].…”

Section: Carbon Monoxide Metabolism and Energy Statusmentioning

confidence: 99%

Carbon Monoxide Targeting Mitochondria

Queiroga

Almeida

Vieira

2012

Biochemistry Research International

View full text Add to dashboard Cite

Mitochondria present two key roles on cellular functioning: (i) cell metabolism, being the main cellular source of energy and (ii) modulation of cell death, by mitochondrial membrane permeabilization. Carbon monoxide (CO) is an endogenously produced gaseoustransmitter, which presents several biological functions and is involved in maintaining cell homeostasis and cytoprotection. Herein, mitochondrion is approached as the main cellular target of carbon monoxide (CO). In this paper, two main perspectives concerning CO modulation of mitochondrial functioning are evaluated. First, the role of CO on cellular metabolism, in particular oxidative phosphorylation, is discussed, namely, on: cytochrome c oxidase activity, mitochondrial respiration, oxygen consumption, mitochondrial biogenesis, and general cellular energetic status. Second, the mitochondrial pathways involved in cell death inhibition by CO are assessed, in particular the control of mitochondrial membrane permeabilization.

show abstract

Metabolic responses in ischemic myocardium after inhalation of carbon monoxide

Abstract: CO in the low-doses tested in this model results in a more favorable energy metabolic condition in that glycolysis is decreased in spite of maintained energy charge. Further work is warranted to clarify the possible mechanistic role of energy metabolism for CO protection.

Cited by 16 publications

References 26 publications

Carbon Monoxide Modulates Apoptosis by Reinforcing Oxidative Metabolism in Astrocytes

Carbon Monoxide Modulates Apoptosis by Reinforcing Oxidative Metabolism in Astrocytes

Heme Oxygenase-1 and Carbon Monoxide in the Heart

Carbon Monoxide Targeting Mitochondria

Contact Info

Product

Resources

About