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dc.contributor.author | Rodríguez-Agudo, Rubén | |
dc.contributor.author | Goikoetxea-Usandizaga, Naroa | |
dc.contributor.author | Serrano-Maciá, Marina | |
dc.contributor.author | Fernández-Tussy, Pablo | |
dc.contributor.author | Fernández-Ramos, David | |
dc.contributor.author | Lachiondo-Ortega, Sofía | |
dc.contributor.author | González-Recio, Irene | |
dc.contributor.author | Gil-Pitarch, Clàudia | |
dc.contributor.author | Mercado-Gómez, María | |
dc.contributor.author | Morán, Laura | |
dc.contributor.author | Bizkarguenaga, Maider | |
dc.contributor.author | Lopitz-Otsoa, Fernando | |
dc.contributor.author | Petrov, Petar | |
dc.contributor.author | Bravo, Miren | |
dc.contributor.author | Van Liempd, Sebastiaan Martijn | |
dc.contributor.author | Falcon-Perez, Juan Manuel | |
dc.contributor.author | Zabala-Letona, Amaia | |
dc.contributor.author | Carracedo, Arkaitz | |
dc.contributor.author | Castell, Jose Vicente | |
dc.contributor.author | Jover, Ramiro | |
dc.contributor.author | Martínez-Cruz, Luis Alfonso | |
dc.contributor.author | Delgado, Teresa Cardoso | |
dc.contributor.author | Cubero, Francisco Javier | |
dc.contributor.author | Lucena, María Isabel | |
dc.contributor.author | Andrade, Raúl Jesús | |
dc.contributor.author | Mabe, Jon | |
dc.contributor.author | Simón, Jorge | |
dc.contributor.author | Martínez-Chantar, María Luz | |
dc.date.accessioned | 2024-02-27T15:07:10Z | |
dc.date.available | 2024-02-27T15:07:10Z | |
dc.date.issued | 2022-04-30 | |
dc.identifier.issn | 2076-3921 | |
dc.identifier.other | http://hdl.handle.net/10668/20781 | |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/18632 | |
dc.description.abstract | Drug-induced liver injury (DILI) development is commonly associated with acetaminophen (APAP) overdose, where glutathione scavenging leads to mitochondrial dysfunction and hepatocyte death. DILI is a severe disorder without effective late-stage treatment, since N-acetyl cysteine must be administered 8 h after overdose to be efficient. Ammonia homeostasis is altered during liver diseases and, during DILI, it is accompanied by decreased glycine N-methyltransferase (GNMT) expression and S-adenosylmethionine (AdoMet) levels that suggest a reduced methionine cycle. Anti-miR-873-5p treatment prevents cell death in primary hepatocytes and the appearance of necrotic areas in liver from APAP-administered mice. In our study, we demonstrate a GNMT and methionine cycle activity restoration by the anti-miR-873-5p that reduces mitochondrial dysfunction and oxidative stress. The lack of hyperammoniemia caused by the therapy results in a decreased urea cycle, enhancing the synthesis of polyamines from ornithine and AdoMet and thus impacting the observed recovery of mitochondria and hepatocyte proliferation for regeneration. In summary, anti-miR-873-5p appears to be an effective therapy against APAP-induced liver injury, where the restoration of GNMT and the methionine cycle may prevent mitochondrial dysfunction while activating hepatocyte proliferative response. | |
dc.language.iso | eng | |
dc.type.hasVersion | VoR | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.subject | acetaminophen (APAP) | |
dc.subject | ammonia | |
dc.subject | drug-induced liver injury (DILI) | |
dc.subject | methionine cycle | |
dc.subject | miR-873-5p | |
dc.subject | mitochondria | |
dc.subject | polyamines | |
dc.subject | therapy | |
dc.title | Methionine Cycle Rewiring by Targeting miR-873-5p Modulates Ammonia Metabolism to Protect the Liver from Acetaminophen. | |
dc.type | research article | |
dc.rights.license | Attribution 4.0 International | * |
dc.identifier.pubmedID | 35624761 | es_ES |
dc.format.volume | 11 | es_ES |
dc.format.number | 5 | es_ES |
dc.identifier.doi | 10.3390/antiox11050897 | |
dc.identifier.journal | Antioxidants (Basel, Switzerland) | es_ES |
dc.rights.accessRights | open access | es_ES |
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IIS BioBizkaia - Asociación Instituto de Investigación Sanitaria BioBizkaia (País Vasco)
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IBIMA-Plataforma BIONAND - Instituto de Investigación Biomédica de Málaga y Plataforma en Nanomedicina (Andalucía)
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