Right-ventricular failure is associated with increased mitochondrial complex II activity and production of reactive oxygen species.

E.M. Redout; M.J. Wagner; M.J. Zuidwijk; C. Boer; R.J.P. Musters; C. van Hardeveld; W.J.S. Paulus; W.S. Simonides

doi:10.1016/j.cardiores.2007.05.012

Right-ventricular failure is associated with increased mitochondrial complex II activity and production of reactive oxygen species.

E.M. Redout
, M.J. Wagner
, M.J. Zuidwijk
, C. Boer
, R.J.P. Musters
, C. van Hardeveld
, W.J.S. Paulus
, W.S. Simonides

Research output: Contribution to Journal › Article › Academic › peer-review

Abstract

Objective: Reactive oxygen species (ROS) have been implicated in the progression of ventricular hypertrophy to congestive heart failure. However, the source of increased oxidative stress in cardiomyocytes remains unclear. Methods: Here we examined NADPH oxidase and mitochondria as sources of ventricular ROS production in a rat model of right-ventricular (RV) failure (CHF) induced by pulmonary arterial hypertension (PAH). Results: Western analysis showed increased expression of the catalytic subunit gp91

Original language	English
Pages (from-to)	770-781
Journal	Cardiovascular Research
Volume	74
DOIs	https://doi.org/10.1016/j.cardiores.2007.05.012
Publication status	Published - 2007

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

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10.1016/j.cardiores.2007.05.012

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title = "Right-ventricular failure is associated with increased mitochondrial complex II activity and production of reactive oxygen species.",

abstract = "Objective: Reactive oxygen species (ROS) have been implicated in the progression of ventricular hypertrophy to congestive heart failure. However, the source of increased oxidative stress in cardiomyocytes remains unclear. Methods: Here we examined NADPH oxidase and mitochondria as sources of ventricular ROS production in a rat model of right-ventricular (RV) failure (CHF) induced by pulmonary arterial hypertension (PAH). Results: Western analysis showed increased expression of the catalytic subunit gp91",

author = "E.M. Redout and M.J. Wagner and M.J. Zuidwijk and C. Boer and R.J.P. Musters and \{van Hardeveld\}, C. and W.J.S. Paulus and W.S. Simonides",

year = "2007",

doi = "10.1016/j.cardiores.2007.05.012",

language = "English",

volume = "74",

pages = "770--781",

journal = "Cardiovascular Research",

issn = "0008-6363",

publisher = "Oxford University Press",

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TY - JOUR

T1 - Right-ventricular failure is associated with increased mitochondrial complex II activity and production of reactive oxygen species.

AU - Redout, E.M.

AU - Wagner, M.J.

AU - Zuidwijk, M.J.

AU - Boer, C.

AU - Musters, R.J.P.

AU - van Hardeveld, C.

AU - Paulus, W.J.S.

AU - Simonides, W.S.

PY - 2007

Y1 - 2007

N2 - Objective: Reactive oxygen species (ROS) have been implicated in the progression of ventricular hypertrophy to congestive heart failure. However, the source of increased oxidative stress in cardiomyocytes remains unclear. Methods: Here we examined NADPH oxidase and mitochondria as sources of ventricular ROS production in a rat model of right-ventricular (RV) failure (CHF) induced by pulmonary arterial hypertension (PAH). Results: Western analysis showed increased expression of the catalytic subunit gp91

AB - Objective: Reactive oxygen species (ROS) have been implicated in the progression of ventricular hypertrophy to congestive heart failure. However, the source of increased oxidative stress in cardiomyocytes remains unclear. Methods: Here we examined NADPH oxidase and mitochondria as sources of ventricular ROS production in a rat model of right-ventricular (RV) failure (CHF) induced by pulmonary arterial hypertension (PAH). Results: Western analysis showed increased expression of the catalytic subunit gp91

U2 - 10.1016/j.cardiores.2007.05.012

DO - 10.1016/j.cardiores.2007.05.012

M3 - Article

SN - 0008-6363

VL - 74

SP - 770

EP - 781

JO - Cardiovascular Research

JF - Cardiovascular Research

ER -

Right-ventricular failure is associated with increased mitochondrial complex II activity and production of reactive oxygen species.

Abstract

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