Pharmacology and Clinical Drug Candidates in Redox Medicine
Open accessAbstract
Significance: Oxidative stress is suggested to be a disease mechanism common to a wide range of disorders affecting human health. However, so far, the pharmacotherapeutic exploitation of this, for example, based on chemical scavenging of pro-oxidant molecules, has been unsuccessful. Recent Advances: An alternative emerging approach is to target the enzymatic sources of disease-relevant oxidative stress. Several such enzymes and isoforms have been identified and linked to different pathologies. For some targets, the respective pharmacology is quite advanced, that is, up to late-stage clinical development or even on the market; for others, drugs are already in clinical use, although not for indications based on oxidative stress, and repurposing seems to be a viable option. Critical Issues: For all other targets, reliable preclinical validation and drug ability are key factors for any translation into the clinic. In this study, specific pharmacological agents with optimal pharmacokinetic profiles are still lacking. Moreover, these enzymes also serve largely unknown physiological functions and their inhibition may lead to unwanted side effects. Future Directions: The current promising data based on new targets, drugs, and drug repurposing are mainly a result of academic efforts. With the availability of optimized compounds and coordinated efforts from academia and industry scientists, unambiguous validation and translation into proof-of-principle studies seem achievable in the very near future, possibly leading towards a new era of redox medicine. Antioxid. Redox Signal. 23, 1113–1129.
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Other proteins related to direct or indirect production of ROS in the cardiovascular system include peroxidases, cyclooxygenases (COX), lipoxygenases, monoamine oxidase, heme oxygenase (HO), glucose oxidase, cytochrome b5 reductase, and CYPOR.
“Other proteins have been related to the direct or indirect production of ROS in the cardiovascular system, including, but not limited to, peroxidases, cyclooxygenases (COX), lipoxygenases, monoamine oxidase, heme oxygenase (HO), glucose oxidase, cytochrome b5 reductase, and CYPOR (209, 505, 790, 908).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [209]
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- Authors
- Dao, V. T.-V., Casas, A. I., Maghzal, G. J., Seredenina, T., Kaludercic, N., Robledinos-Anton, N., Di Lisa, F., Stocker, R., Ghezzi, P., Jaquet, V., Cuadrado, A., & Schmidt, H. H. H. W.
- Affiliations
- Maastricht University (NL)
- Victor Chang Cardiac Research Institute (AU)
- University of Geneva (CH)
- National Research Council (IT)
- Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)
- Neuroscience Institute
- Brighton and Sussex Medical School (GB)
- Consejo Superior de Investigaciones Científicas (ES)
- Corresponding author
- Dao, V. Thao-Vi
- ORCID
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2015-11
- Volume
- 23
- Issue
- 14
- Pages
- 1113-1129
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- PMC
- PMC4657508
- OpenAlex
- W2147975677
- Cited by
- 88
- References
- 171
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 7 · 2022: 8 · 2021: 7 · 2020: 18 · 2019: 7 · 2018: 6 · 2017: 16 · 2016: 10 · 2015: 1
- FWCI
- 1.07
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Antioxidants and Redox Signaling (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion, other-oa)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Sussex Research Online (University of Sussex) (submittedVersion, cc-by-nc)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, cc-by-nc)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Figshare (submittedVersion, cc-by-nc)
- CINECA IRIS Institutional Research information system (University of Urbino) (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Padua Research Archive (University of Padova) (submittedVersion, cc-by-nc)
- Funders
- Sanofi
- European Foundation for the Study of Diabetes
- Universiteit Maastricht
- National Health and Medical Research Council
- CARIM School for Cardiovascular Diseases, Universiteit Maastricht
- Eurostars
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- oxidative stress, oxidative enzymes, enzyme inhibition, drug repurposing, pharmacology, clinical drug candidates, pharmacokinetics, adverse effects, preclinical validation
- MeSH terms
- Animals, Antioxidants, Drug Evaluation, Preclinical, Enzyme Inhibitors, Humans, Oxidation-Reduction, Drug Design, Reactive Oxygen Species, Oxidative Stress
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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