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

Title: Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases
Authors: Rojo, Ana I; Buttari, Brigitta; Cadenas, Susana; Carlos, Ana Rita; Cuadrado, Antonio; Falcão, Ana Sofia; López, Manuela G; Georgiev, Milen I; Grochot-Przeczek, Anna; Gumeni, Sentiljana; Jimenez-Villegas, José; Horbanczuk, Jarosław Olav; Konu, Ozlen; Lastres-Becker, Isabel; Levonen, Anna-Liisa; Maksimova, Viktorija; Michaeloudes, Charalambos; Mihaylova, Liliya V; Mickael, Michel Edwar; Milisav, Irina; Miova, Biljana; Rada, Patricia; Santos, Marlene; Seabra, Miguel C; Strac, Dubravka Svob; Tenreiro, Sandra; Trougakos, Ioannis P; Dinkova-Kostova, Albena T
Contributors: Ministerio de Ciencia, Innovación y Universidades (España); Agencia Estatal de Investigación (España); Comunidad de Madrid; Fundación la Caixa; Instituto de Salud Carlos III; Bulgarian National Science Fund; European Commission; Medical Research Council (UK); Biotechnology and Biological Sciences Research Council (UK); European Cooperation in Science and Technology; Consejo Superior de Investigaciones Científicas https://ror.org/02gfc7t72
Publisher Information: Elsevier
Publication Year: 2025
Collection: Digital.CSIC (Consejo Superior de Investigaciones Científicas / Spanish National Research Council)
Subject Terms: Inflammation; Model organisms; NRF2; Non-communicable chronic diseases; Oxidative stress
Description: Non-communicable chronic diseases (NCDs) are most commonly characterized by age-related 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. ; Research 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 ...
Document Type: article in journal/newspaper
Language: English
Relation: #PLACEHOLDER_PARENT_METADATA_VALUE#; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2019-110061RB-I00/ES/EL FACTOR DE TRANSCRIPCION NRF2 EN LA PATOFISIOLOGIA DE LA ENFERMEDAD DE ALZHEIMER/; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PDC2021-121421-I00/ES/DESARROLLO DE NUEVOS FARMACOS ANTI-INFLAMATORIOS BASADOS EN LA ACTIVACION DEL FACTOR DE TRANSCRIPCION NRF2/; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2021-2023/PDC2022-133765-I00/ES/OPTIMIZACION DE UN NUEVO ACTIVADOR DEL FACTOR DE TRANSCRIPCION NRF2 PARA FRENAR LA PROGRESION DE NASH/; Sí; Redox Biol . 2025 Feb:79:103464.; https://hdl.handle.net/10261/398195; http://dx.doi.org/10.13039/501100003336; http://dx.doi.org/10.13039/501100011033; http://dx.doi.org/10.13039/501100000268; http://dx.doi.org/10.13039/501100004587; http://dx.doi.org/10.13039/501100000265; http://dx.doi.org/10.13039/100012818; http://dx.doi.org/10.13039/501100000780; http://dx.doi.org/10.13039/501100000921
DOI: 10.13039/501100003336
DOI: 10.13039/501100011033
DOI: 10.13039/501100000268
DOI: 10.13039/501100004587
DOI: 10.13039/501100000265
DOI: 10.13039/100012818
DOI: 10.13039/501100000780
DOI: 10.13039/501100000921
Availability: https://hdl.handle.net/10261/398195; https://doi.org/10.13039/501100003336; https://doi.org/10.13039/501100011033; https://doi.org/10.13039/501100000268; https://doi.org/10.13039/501100004587; https://doi.org/10.13039/501100000265; https://doi.org/10.13039/100012818; https://doi.org/10.13039/501100000780; https://doi.org/10.13039/501100000921
Rights: info:eu-repo/semantics/openAccess
Accession Number: edsbas.3D22A11F
Database: BASE