Human Nitric Oxide Synthase—Its Functions, Polymorphisms, and Inhibitors in the Context of Inflammation, Diabetes and Cardiovascular Diseases
Open accessAbstract
In various diseases, there is an increased production of the free radicals needed to carry out certain physiological processes but their excessive amounts can cause oxidative stress and cell damage. Enzymes play a major role in the transformations associated with free radicals. One of them is nitric oxide synthase (NOS), which catalyzes the formation of nitric oxide (NO). This enzyme exists in three forms (NOS1, NOS2, NOS3), each encoded by a different gene. The following work presents the most important information on the NOS isoforms and their role in the human body, including NO synthesis in various tissues and cells, intercellular signaling and activities supporting the immune system and regulating blood vessel functions. The role of NOS in pathological conditions such as obesity, diabetes and heart disease is considered. Attention is also paid to the influence of the polymorphisms of these genes, encoding particular isoforms, on the development of these pathologies and the role of NOS inhibitors in the treatment of patients.
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Nitric oxide, a metabolite of L-arginine, has a role in sexual functions.
“Nitric oxide is one of the metabolites of L-arginine, which has many activities in the body, including its role in sexual functions [29].”
From Effect of l-arginine compared to placebo on sexual function in women with major depressive disorder: a randomized controlled trial (2024) · cites this paper as [29]
Section 2, “Characteristics of NO and Its Derivatives” (page unavailable), says NO is formed from arginine by nitric oxide synthase. Section 5, “Selected NOS Inhibitors and Their Role in Therapy” (page unavailable), describes NO’s role in genitourinary neurotransmission, but the passages do not specifically address sexual functions. (LLM, conf=0.83)
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Background
- Authors
- Król, M., & Kepinska, M.
- Affiliations
- Department of Biomedical and Environmental Analyses, Faculty of Pharmacy, Wroclaw Medical University, Borowska 211, 50-556 Wroclaw, Poland
- ORCID
- Kepinska, Marta
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-12-23
- Volume
- 22
- Issue
- 1
- Pages
- 56
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7793075
- OpenAlex
- W3117397075
- Cited by
- 187
- References
- 141
- Citations by year
- 2026: 25 · 2025: 44 · 2024: 33 · 2023: 44 · 2022: 26 · 2021: 15
- FWCI
- 2.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Ministerstwo Nauki i Szkolnictwa Wyższego (016/RID/2018/19)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Keywords
- nitric oxide synthase, nitric oxide, NOS isoforms, NOS1, NOS2, NOS3, genetic polymorphism, nitric oxide synthase inhibitors, inflammation, diabetes mellitus, cardiovascular disease, obesity, oxidative stress, intercellular communication, immune system, vascular function
- MeSH terms
- Animals, Cardiovascular Diseases, Diabetes Mellitus, Disease Susceptibility, Enzyme Activation, Enzyme Inhibitors, Humans, Inflammation, Insulin Resistance, Isoenzymes, Nitric Oxide, Obesity, Polymorphism, Genetic, Structure-Activity Relationship, Oxidative Stress, Nitric Oxide Synthase, Polymorphism, Single Nucleotide, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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