Key result
NOX5 expression increases ROS production to exaggerate cardiac hypertrophy and contractile dysfunction during pressure overload.
Why the study?
The function of NOX5 in cardiac hypertrophy and its role in oxidative stress-mediated cardiac remodeling and dysfunction were unknown.
Does NOX5 overexpression exacerbate cardiac hypertrophy and contractile dysfunction in preclinical models?
Population
Cardiac tissue from patients with cardiomyopathy and heart failure, rat cardiomyocytes, and NOX5 transgenic mice
Comparison
NOX5 overexpression with Ang II or pressure overload versus controls without NOX5 overexpression
Design
Preclinical experimental study using human tissue, cell culture, and transgenic mouse models
Authors
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NOX5 may drive oxidative hypertrophy in preclinical overload; leaves open targeted inhibition in human hypertensive heart disease.
Does NOX5 overexpression exacerbate cardiac hypertrophy and contractile dysfunction in preclinical models?
Ca2+-regulated NOX5 is an important isoform involved in oxidative stress- and MAPK-mediated cardiac hypertrophy and contractile dysfunction.
Zhao et al. (2020) studied Cardiac hypertrophy. NOX5 expression vs. Control was evaluated on Cardiac hypertrophy and contractile dysfunction. Ca2+-regulated NOX5 expression increased reactive oxygen species production and exaggerated cardiac hypertrophy and contractile dysfunction in response to pressure overload and Angiotensin II.
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