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Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver

Idelfonso-García, Osiris Germán ; Alarcón-Sánchez, Brisa Rodope ; Guerrero-Escalera, Dafne ; López-Hernández, Norma Arely ; Pérez-Hernández, José Luis ; Pacheco-Rivera, Ruth ; Serrano-Luna, Jesús ; Resendis-Antonio, Osbaldo ; Muciño-Olmos, Erick Andrés LU orcid and Aparicio-Bautista, Diana Ivette , et al. (2024) In Antioxidants 13(3).
Abstract

Aging is characterized by increased reactive species, leading to redox imbalance, oxidative damage, and senescence. The adverse effects of alcohol consumption potentiate aging-associated alterations, promoting several diseases, including liver diseases. Nucleoredoxin (NXN) is a redox-sensitive enzyme that targets reactive oxygen species and regulates key cellular processes through redox protein–protein interactions. Here, we determine the effect of chronic alcohol consumption on NXN-dependent redox interactions in the liver of aged mice. We found that chronic alcohol consumption preferentially promotes the localization of NXN either into or alongside senescent cells, declines its interacting capability, and worsens the altered... (More)

Aging is characterized by increased reactive species, leading to redox imbalance, oxidative damage, and senescence. The adverse effects of alcohol consumption potentiate aging-associated alterations, promoting several diseases, including liver diseases. Nucleoredoxin (NXN) is a redox-sensitive enzyme that targets reactive oxygen species and regulates key cellular processes through redox protein–protein interactions. Here, we determine the effect of chronic alcohol consumption on NXN-dependent redox interactions in the liver of aged mice. We found that chronic alcohol consumption preferentially promotes the localization of NXN either into or alongside senescent cells, declines its interacting capability, and worsens the altered interaction ratio of NXN with FLII, MYD88, CAMK2A, and PFK1 proteins induced by aging. In addition, carbonylated protein and cell proliferation increased, and the ratios of collagen I and collagen III were inverted. Thus, we demonstrate an emerging phenomenon associated with altered redox homeostasis during aging, as shown by the declining capability of NXN to interact with partner proteins, which is enhanced by chronic alcohol consumption in the mouse liver. This evidence opens an attractive window to elucidate the consequences of both aging and chronic alcohol consumption on the downstream signaling pathways regulated by NXN-dependent redox-sensitive interactions.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
alcoholic liver disease, cellular senescence, oxidative stress, protein carbonylation
in
Antioxidants
volume
13
issue
3
article number
257
publisher
MDPI AG
external identifiers
  • pmid:38539791
  • scopus:85188738157
ISSN
2076-3921
DOI
10.3390/antiox13030257
language
English
LU publication?
yes
id
dc7199cd-c808-48a3-b718-69fa978ae6ab
date added to LUP
2024-04-12 07:57:44
date last changed
2024-04-26 09:52:24
@article{dc7199cd-c808-48a3-b718-69fa978ae6ab,
  abstract     = {{<p>Aging is characterized by increased reactive species, leading to redox imbalance, oxidative damage, and senescence. The adverse effects of alcohol consumption potentiate aging-associated alterations, promoting several diseases, including liver diseases. Nucleoredoxin (NXN) is a redox-sensitive enzyme that targets reactive oxygen species and regulates key cellular processes through redox protein–protein interactions. Here, we determine the effect of chronic alcohol consumption on NXN-dependent redox interactions in the liver of aged mice. We found that chronic alcohol consumption preferentially promotes the localization of NXN either into or alongside senescent cells, declines its interacting capability, and worsens the altered interaction ratio of NXN with FLII, MYD88, CAMK2A, and PFK1 proteins induced by aging. In addition, carbonylated protein and cell proliferation increased, and the ratios of collagen I and collagen III were inverted. Thus, we demonstrate an emerging phenomenon associated with altered redox homeostasis during aging, as shown by the declining capability of NXN to interact with partner proteins, which is enhanced by chronic alcohol consumption in the mouse liver. This evidence opens an attractive window to elucidate the consequences of both aging and chronic alcohol consumption on the downstream signaling pathways regulated by NXN-dependent redox-sensitive interactions.</p>}},
  author       = {{Idelfonso-García, Osiris Germán and Alarcón-Sánchez, Brisa Rodope and Guerrero-Escalera, Dafne and López-Hernández, Norma Arely and Pérez-Hernández, José Luis and Pacheco-Rivera, Ruth and Serrano-Luna, Jesús and Resendis-Antonio, Osbaldo and Muciño-Olmos, Erick Andrés and Aparicio-Bautista, Diana Ivette and Basurto-Islas, Gustavo and Baltiérrez-Hoyos, Rafael and Vásquez-Garzón, Verónica Rocío and Villa-Treviño, Saúl and Muriel, Pablo and Serrano, Héctor and Pérez-Carreón, Julio Isael and Arellanes-Robledo, Jaime}},
  issn         = {{2076-3921}},
  keywords     = {{alcoholic liver disease; cellular senescence; oxidative stress; protein carbonylation}},
  language     = {{eng}},
  number       = {{3}},
  publisher    = {{MDPI AG}},
  series       = {{Antioxidants}},
  title        = {{Nucleoredoxin Redox Interactions Are Sensitized by Aging and Potentiated by Chronic Alcohol Consumption in the Mouse Liver}},
  url          = {{http://dx.doi.org/10.3390/antiox13030257}},
  doi          = {{10.3390/antiox13030257}},
  volume       = {{13}},
  year         = {{2024}},
}