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Difference between revisions of "Wilson 2018 Virginia Tech"

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|title=Wilson ZT, Perry JB, Brow DA (2018) High-resolution respirometry of heart mitochondria in healthy and stressed states. Virginia Tech.
|title=Wilson ZT, Perry JB, Brow DA (2018) High-resolution respirometry of heart mitochondria in healthy and stressed states. Virginia Tech.
|info=[https://vtechworks.lib.vt.edu/handle/10919/84553 VTechWorks]
|info=[https://vtechworks.lib.vt.edu/handle/10919/84553 VTechWorks]
|authors=Wilson ZT, Perry JB, Brow DA
|authors=Wilson ZT, Perry JB, Brown DA
|year=2018
|year=2018
|event=Virginia Tech
|event=Virginia Tech
|abstract=Heart disease remains the leading cause of death globally, claiming the lives of nearly 10 million people in 2016. Current standard-of-care therapies for heart disease patients reduce energy demands on the heart but do not treat underlying deficits in cellular energy production. Cardiac mitochondria are primarily responsible for the production of energy in the heart, and targeting dysfunctional mitochondria represents a promising solution to improving the prognosis of heart disease patients. Increased production of reactive oxygen species in heart disease damages mitochondrial function, ultimately decreasing cardiac energy supply. Isolated mitochondria exposed to hydrogen peroxide serves as a heart disease model where the reactive oxygen species damage the respiratory chain, a series of complexes responsible for the actual production of energy. N-acetylcysteine (NAC) is a drug precursor to glutathione, an endogenous antioxidant which reduces reactive oxygen species. In this project, isolated mitochondria are treated with hydrogen peroxide with or without NAC. If NAC is capable of rescuing the respiratory rate, that would suggest that NAC restores mitochondrial energy production in pathological states. If successful, these data would be the first step in determining if incorporation of NAC into heart disease treatment plans could begin to better treat the number of one cause of morbidity/mortality on the planet.
|abstract=Heart disease remains the leading cause of death globally, claiming the lives of nearly 10 million people in 2016. Current standard-of-care therapies for heart disease patients reduce energy demands on the heart but do not treat underlying deficits in cellular energy production. Cardiac mitochondria are primarily responsible for the production of energy in the heart, and targeting dysfunctional mitochondria represents a promising solution to improving the prognosis of heart disease patients. Increased production of reactive oxygen species in heart disease damages mitochondrial function, ultimately decreasing cardiac energy supply. Isolated mitochondria exposed to hydrogen peroxide serves as a heart disease model where the reactive oxygen species damage the respiratory chain, a series of complexes responsible for the actual production of energy. N-acetylcysteine (NAC) is a drug precursor to glutathione, an endogenous antioxidant which reduces reactive oxygen species. In this project, isolated mitochondria are treated with hydrogen peroxide with or without NAC. If NAC is capable of rescuing the respiratory rate, that would suggest that NAC restores mitochondrial energy production in pathological states. If successful, these data would be the first step in determining if incorporation of NAC into heart disease treatment plans could begin to better treat the number of one cause of morbidity/mortality on the planet.
|editor=[[Plangger M]], [[Kandolf G]],
|editor=[[Plangger M]], [[Kandolf G]],
|mipnetlab=US NC Greenville Brown DA
}}
}}
{{Labeling
{{Labeling

Latest revision as of 14:49, 22 August 2018

Wilson ZT, Perry JB, Brow DA (2018) High-resolution respirometry of heart mitochondria in healthy and stressed states. Virginia Tech.

Link: VTechWorks

Wilson ZT, Perry JB, Brown DA (2018)

Event: Virginia Tech

Heart disease remains the leading cause of death globally, claiming the lives of nearly 10 million people in 2016. Current standard-of-care therapies for heart disease patients reduce energy demands on the heart but do not treat underlying deficits in cellular energy production. Cardiac mitochondria are primarily responsible for the production of energy in the heart, and targeting dysfunctional mitochondria represents a promising solution to improving the prognosis of heart disease patients. Increased production of reactive oxygen species in heart disease damages mitochondrial function, ultimately decreasing cardiac energy supply. Isolated mitochondria exposed to hydrogen peroxide serves as a heart disease model where the reactive oxygen species damage the respiratory chain, a series of complexes responsible for the actual production of energy. N-acetylcysteine (NAC) is a drug precursor to glutathione, an endogenous antioxidant which reduces reactive oxygen species. In this project, isolated mitochondria are treated with hydrogen peroxide with or without NAC. If NAC is capable of rescuing the respiratory rate, that would suggest that NAC restores mitochondrial energy production in pathological states. If successful, these data would be the first step in determining if incorporation of NAC into heart disease treatment plans could begin to better treat the number of one cause of morbidity/mortality on the planet.


β€’ Bioblast editor: Plangger M, Kandolf G β€’ O2k-Network Lab: US NC Greenville Brown DA


Labels: MiParea: Respiration, Pharmacology;toxicology  Pathology: Cardiovascular  Stress:Temperature 

Tissue;cell: Heart  Preparation: Isolated mitochondria 


Coupling state: OXPHOS  Pathway:HRR: Oxygraph-2k 


Affiliations

Dept Human Nutrition, Foods, and Exercise, Virginia Tech, Blacksburg, VA, USA

Figures

Wilson 2018 Virginia Tech Poster.jpg












Acknowledgement

Funding for the TOUR Scholars program provided by the Department of Human Nutrition, Foods, and Exercise, the College of Agriculture and Life Sciences, The Obesity Interdisciplinary Graduate Education Program, and the Center for Transformative Research on Health Behaviors, and is under the direction of Dr. Deborah J. Good and Dr. Samantha M. Harden. This research was supported by NIH NHLBI RO1 HL123647.