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Updated: May 24, 2026
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Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
Published on: February 16, 2022
Dynamic denitrosylation via S-nitrosoglutathione reductase regulates cardiovascular function
Farideh Beigi1, Daniel R Gonzalez, Khalid M Minhas
1Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Summary
Protein denitrosylation, mediated by S-nitrosoglutathione reductase (GSNOR), regulates vascular tone and cardiac function. GSNOR deficiency impairs these responses, highlighting denitrosylation
Area of Science:
- Cardiovascular Physiology
- Biochemistry
- Nitric Oxide Signaling
Background:
- Protein S-nitrosylation is a key nitric oxide (NO) signaling mechanism.
- The physiological roles of protein denitrosylation remain largely unexplored.
- S-nitrosoglutathione reductase (GSNOR) is a primary enzyme regulating protein denitrosylation.
Purpose of the Study:
- To investigate the physiological functions of protein denitrosylation.
- To determine the role of GSNOR in regulating cardiovascular function.
- To elucidate the mechanisms underlying GSNOR-mediated cardiovascular regulation.
Main Methods:
- Utilized GSNOR-deficient mouse models.
- Assessed peripheral vascular tone and cardiac contractility.
- Analyzed protein denitrosylation of cardiac ryanodine receptor 2 (RyR2) following beta-adrenergic stimulation.
Main Results:
- GSNOR deficiency led to reduced peripheral vascular tone.
- GSNOR-deficient mice showed depressed cardiac contractility in response to beta-adrenergic agonists.
- Impaired denitrosylation of RyR2 in GSNOR-deficient hearts resulted in calcium leak.
- Aberrant denitrosylation was linked to impaired cardiovascular function.
Conclusions:
- Protein denitrosylation, regulated by GSNOR, is essential for cardiovascular homeostasis.
- GSNOR and NO synthase act in concert to regulate hemodynamic responses.
- Dysregulation of protein denitrosylation contributes to cardiovascular dysfunction.
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