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Altered NRF2 signalling in systemic redox imbalance: Insights from non-communicable diseases

dc.contributor.authorSantos, Marlene
dc.contributor.authorMorgenstern, Christina
dc.contributor.authorSantos, Marlene
dc.date.accessioned2025-10-21T10:16:44Z
dc.date.available2025-10-21T10:16:44Z
dc.date.issued2025-10-10
dc.description.abstractThe balanced activity of the cytoprotective transcription factor NRF2 is central for maintaining redox, metabolic-energetics, and proteome homeostasis, as well as for regulating inflammatory responses, among other functions. Activated NRF2 regulates the expression of hundreds of genes containing antioxidant response elements (AREs) or electrophile response elements (EpRE) in their regulatory regions, often promoting cytoprotection under stress conditions and contributing to defence against various pathologies and non-communicable diseases (NCDs). The products of increased NRF2 activity, detected systemically, may originate from either the white blood cells, the cells of the vasculature or tissue-derived products that could be secreted into biological fluids. Therefore, assessing basal and inducible NRF2 activity in blood or other biofluids is crucial for inferring NRF2 responses in local and often inaccessible tissues. In previous work, we identified a panel of six biomarkers - Glutamate-cysteine ligase catalytic subunit (GCLC), Glutamate-cysteine ligase modifier subunit (GCLM), Haem oxygenase 1 (HMOX1), NAD(P)H quinone dehydrogenase 1 (NQO1), Sulfiredoxin 1 (SRXN1), and Thioredoxin reductase 1 (TXNRD1) - as indicators of NRF2 activity. In the current study, we assess their utility in a clinical setting to measure NRF2 activation in a disease context. Here we discuss findings on how NRF2 activity in accessible human samples can reveal its involvement in various NCDs and its connection to clinical aspects such as diagnosis, disease progression and response to therapy.por
dc.identifier.citationJakubowska, M., Costa, V. M., Krzeptowski, W., Dominkuš, P. P., Santos, M., Demirdöğen, B. C., Genç, Ş., Trougakos, I. P., Kanninen, K. M., Winklhofer-Roob, B. M., Copple, I. M., Cuadrado, A., Dolžan, V., & Morgenstern, C. (2025). Altered NRF2 signalling in systemic redox imbalance: Insights from non-communicable diseases. Redox Biology, 87, 103891. https://doi.org/10.1016/j.redox.2025.103891
dc.identifier.doi10.1016/j.redox.2025.103891
dc.identifier.issn2213-2317
dc.identifier.urihttp://hdl.handle.net/10400.22/30655
dc.language.isoeng
dc.peerreviewedyes
dc.publisherElsevier
dc.relation.hasversionhttps://www.sciencedirect.com/science/article/pii/S2213231725004045?via%3Dihub
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectBiomarker
dc.subjectNRF2
dc.subjectNon-communicable diseases
dc.subjectRedox imbalance
dc.subjectOxidative stress
dc.subjectTranscription factor
dc.titleAltered NRF2 signalling in systemic redox imbalance: Insights from non-communicable diseasespor
dc.typeresearch article
dspace.entity.typePublication
oaire.citation.titleRedox Biology
oaire.versionhttp://purl.org/coar/version/c_970fb48d4fbd8a85
person.familyNameSantos
person.givenNameMarlene
person.identifier1508370
person.identifier.ciencia-id8311-B967-31C4
person.identifier.orcid0000-0001-5020-5942
person.identifier.scopus-author-id57110502000
relation.isAuthorOfPublication8ce9ee39-a4c6-46ae-99e2-49397b550f1b
relation.isAuthorOfPublication.latestForDiscovery8ce9ee39-a4c6-46ae-99e2-49397b550f1b

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