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Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases

dc.contributor.authorRojo, Ana I.
dc.contributor.authorButtari, Brigitta
dc.contributor.authorCadenas, Susana
dc.contributor.authorCarlos, Ana Rita
dc.contributor.authorCuadrado, Antonio
dc.contributor.authorFalcão, Ana Sofia
dc.contributor.authorLópez, Manuela G.
dc.contributor.authorGeorgiev, Milen I.
dc.contributor.authorGrochot-Przeczek, Anna
dc.contributor.authorGumeni, Sentiljana
dc.contributor.authorJimenez-Villegas, José
dc.contributor.authorHorbanczuk, Jarosław Olav
dc.contributor.authorKonu, Ozlen
dc.contributor.authorLastres-Becker, Isabel
dc.contributor.authorLevonen, Anna-Liisa
dc.contributor.authorMaksimova, Viktorija
dc.contributor.authorMichaeloudes, Charalambos
dc.contributor.authorMihaylova, Liliya V.
dc.contributor.authorMickael, Michel Edwar
dc.contributor.authorMilisav, Irina
dc.contributor.authorMiova, Biljana
dc.contributor.authorRada, Patricia
dc.contributor.authorSantos, Marlene
dc.contributor.authorSeabra, Miguel C.
dc.contributor.authorStrac, Dubravka Svob
dc.contributor.authorTenreiro, Sandra
dc.contributor.authorTrougakos, Ioannis P.
dc.contributor.authorDinkova-Kostova, Albena T.
dc.date.accessioned2024-12-23T09:14:12Z
dc.date.available2024-12-23T09:14:12Z
dc.date.issued2024-12-16
dc.description.abstractNon-communicable chronic diseases (NCDs) are most commonly characterized by agerelated loss of homeostasis and/or by cumulative exposures to environmental factors, which lead to low-grade sustained generation of reactive oxygen species (ROS), chronic inflammation and metabolic imbalance. Nuclear factor erythroid 2-like 2 (NRF2) is a basic leucine-zipper transcription factor that regulates the cellular redox homeostasis. NRF2 controls the expression of more than 250 human genes that share in their regulatory regions a cis-acting enhancer termed the antioxidant response element (ARE). The products of these genes participate in numerous functions including biotransformation and redox homeostasis, lipid and iron metabolism, inflammation, proteostasis, as well as mitochondrial dynamics and energetics. Thus, it is possible that a single pharmacological NRF2 modulator might mitigate the effect of the main hallmarks of NCDs, including oxidative, proteostatic, inflammatory and/or metabolic stress. Research on model organisms has provided tremendous knowledge of the molecular mechanisms by which NRF2 affects NCDs pathogenesis. This review is a comprehensive summary of the most commonly used model organisms of NCDs in which NRF2 has been genetically or pharmacologically modulated, paving the way for drug development to combat NCDs. We discuss the validity and use of these models and identify future challenges.pt_PT
dc.description.versioninfo:eu-repo/semantics/acceptedVersionpt_PT
dc.identifier.citationRojo, A. I., Buttari, B., Cadenas, S., Carlos, A. R., Cuadrado, A., Falcão, A. S., López, M. G., Georgiev, M. I., Grochot-Przeczek, A., Gumeni, S., Jimenez-Villegas, J., Horbanczuk, J. O., Konu, O., Lastres-Becker, I., Levonen, A.-L., Maksimova, V., Michaeloudes, C., Mihaylova, L. V., Mickael, M. E., … Dinkova-Kostova, A. T. (2024). Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases. Redox Biology, 103464. https://doi.org/10.1016/j.redox.2024.103464pt_PT
dc.identifier.doi10.1016/j.redox.2024.103464pt_PT
dc.identifier.eissn2213-2317
dc.identifier.urihttp://hdl.handle.net/10400.22/26918
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherElsevierpt_PT
dc.relationResearch in the authors’ laboratories is funded as follows: AIR and AC by the Spanish Ministry of Science, Innovation and Universities (PID2019-110061RB-I00, PID-2021-122766OB-100, PDC2021-121421-I00, PDC2022-133765-I00), CIBERNED/ISCIII (CB06/05/0010), and The Autonomous Community of Madrid (P2022/BMD-7230). MGL is funded by Spanish Ministry of Science, Innovation and Universities (PID2021-125986OB-I00, PDC2022-133809-I00) and Community of Madrid Ref. P2022/BMD-7230-CAM-22. PR is funded by Spanish Ministry of Science, Innovation and Universities (PID2023-150994OB-I00), The Autonomous Community of Madrid (P2022/BMD-7227) and CIBERDEM/ISCIII (CB07/08/0033). JJV is holder of a FPU contract of Spanish Ministry of Science, Innovation and Universities (FPU20/03326). ILB is funded by the Spanish Ministry of Science, Innovation and Universities (PID2022-137065OB-100, PCD2022-133774-100) and CIBERNED/ISCIII (CB06/05/0089). MCS, ST and ASF are funded by Fundação para a Ciência e a Tecnologia through R&D unit iNOVA4Health (UIDB/04462/2020 and UIDP/04462/2020) and LS4FUTURE Associated Laboratory (LA/P/0087/2020). ASF is holder of a post-doctoral contract from “La Caixa Foundation” (NASCENT HR22-00569). IM received research core funding by Slovenian Research Agency (P3-0019). AG received research funding from the National Science Centre grant OPUS (2021/43/B/NZ4/02130). ARC is supported by the donor Henrique Meirelles who chose to support the MATRIHEALTH Project (CC1036), Fundação para a Ciência e a Tecnologia Project (http://dx.doi.org/10.54499/PTDC/BTM-ORG/1383/2020) and Unit Funding (http://dx.doi.org/10.54499/UIDB/00329/2020). IPT acknowledges funding from NKUA SARG (C.S. 19067). SC is funded by the ISCIII (PI23/01846). LVM is a grant holder of a contract КП-06-КОСТ/4 of the Bulgarian National Science Fund under BG-175467353-2023-03 programme. LVM and MIG have received funding from the European Union’s Horizon 2020 research and innovation programme, project PlantaSYST (SGA No 739582 under FPA No. 664620) and by the European Regional Development Fund through the Bulgarian “Science and Education for Smart Growth” Operational Programme (BG05M2OP001-1.003-001-C01) and Programme Research Innovation and Digitalisation for Smart Transformation. OK is funded by the European Union Horizon's research and innovation program HORIZON-HLTH-2022-STAYHLTH-02 under agreement No 101095679. ADK is funded by the Medical Research Council UK (MR/W023806/1), the Biotechnology and Biological Sciences Research Council UK (BB/T508111/1 and BB/X00029X/1), Tenovus Scotland (T22-08), and the Cunnigham Trust. This article is based upon work from COST Action CA20121, supported by COST (European Cooperation in Science and Technology) (www.cost.eu) (https://benbedphar.org/about-benbedphar/).pt_PT
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S2213231724004427?via%3Dihubpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/pt_PT
dc.subjectInflammationpt_PT
dc.subjectModel organismspt_PT
dc.subjectNon-communicable chronic diseasespt_PT
dc.subjectNRF2pt_PT
dc.subjectOxidative stresspt_PT
dc.titleModel organisms for investigating the functional involvement of NRF2 in non-communicable diseasespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.titleRedox Biologypt_PT
person.familyNameSantos
person.givenNameMarlene
person.identifier1508370
person.identifier.ciencia-id8311-B967-31C4
person.identifier.orcid0000-0001-5020-5942
person.identifier.scopus-author-id57110502000
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication8ce9ee39-a4c6-46ae-99e2-49397b550f1b
relation.isAuthorOfPublication.latestForDiscovery8ce9ee39-a4c6-46ae-99e2-49397b550f1b

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