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NADPH Oxidases in Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction
James P Teuber1, Kobina Essandoh1, Scott L Hummel2,3
1Department of Pharmacology, University of Michigan, Ann Arbor, MI 48109, USA.
Antioxidants (Basel, Switzerland)
|September 23, 2022
Summary
Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases are crucial for cardiovascular health, regulating reactive oxygen species (ROS) and signaling. Their dysfunction contributes to heart failure with preserved ejection fraction (HFpEF) and diastolic dysfunction.
Area of Science:
- Cardiovascular Biology
- Oxidative Stress Research
- Molecular Medicine
Background:
- Nicotinamide adenine dinucleotide phosphate (NADPH) oxidases generate reactive oxygen species (ROS), impacting cellular redox signaling and oxidative damage.
- NADPH oxidase (NOX) enzymes are implicated in regulating intracellular signaling within various cardiovascular cell types.
- NOX2 and NOX4 specifically influence cardiac myocyte redox signaling, affecting cardiac hypertrophy and heart failure progression.
Purpose of the Study:
- To elucidate the role of NOX enzymes in the development and progression of diastolic dysfunction and heart failure with preserved ejection fraction (HFpEF).
- To explore the involvement of NOX enzymes in HFpEF-associated systemic pathologies and cardiovascular cell dysfunction.
- To discuss potential clinical implications of NOX enzyme activity in HFpEF.
Main Methods:
- Review of existing research on NOX enzyme mechanisms in cardiovascular cells.
- Analysis of basic science studies and clinical data linking oxidative stress to HFpEF.
- Examination of evidence from animal models demonstrating NOX enzyme functions in diastolic function and HFpEF comorbidities.
Main Results:
- NADPH oxidase enzymes play critical roles in regulating oxidative stress and redox signaling in cardiovascular cells.
- NOX enzymes are implicated in the pathogenesis of diastolic dysfunction and heart failure with preserved ejection fraction.
- Evidence supports the involvement of NOX enzymes in multiple organ system dysfunctions associated with HFpEF.
Conclusions:
- NOX enzymes are key regulators of cardiovascular cell function and are critically involved in the pathophysiology of HFpEF.
- Targeting NOX enzymes may offer therapeutic strategies for managing diastolic dysfunction and HFpEF.
- Further research into NOX enzyme pathways is warranted for clinical applications in heart failure treatment.
Keywords:
HFpEFNADPH oxidasesNOX2NOX4RAASROSRac1S-nitrosylationangiotensincardiac hypertrophycardiomyopathydiastolic dysfunctionheart failurenitrosative stressoxidative stressredox signalingMore Related Videos
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