| Autor: |
Idelfonso-García OG; Laboratory of Liver Diseases, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico.; Department of Health Sciences, Div CBS, Metropolitan Autonomous University-Iztapalapa Campus, Mexico City 09340, Mexico., Alarcón-Sánchez BR; Laboratory of Liver Diseases, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico.; Department of Cell Biology, Center for Research and Advanced Studies of the National Polytechnic Institute-CINVESTAV-IPN, Mexico City 07360, Mexico., Guerrero-Escalera D; Laboratory of Liver Diseases, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico., López-Hernández NA; Laboratory of Liver Diseases, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico., Pérez-Hernández JL; Department of Gastroenterology and Hepatology, Hospital General de México 'Dr. Eduardo Liceaga', Mexico City 06720, Mexico., Pacheco-Rivera R; Laboratory of Molecular Diagnostics, Department of Biochemistry, National School of Biological Sciences of the National Polytechnic Institute, Mexico City 07738, Mexico., Serrano-Luna J; Department of Cell Biology, Center for Research and Advanced Studies of the National Polytechnic Institute-CINVESTAV-IPN, Mexico City 07360, Mexico., Resendis-Antonio O; Laboratory of Human Systems Biology, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico.; Coordination of Scientific Research-CIC, Research Support Network-RAI, Center for Complexity Sciences-C3, National Autonomous University of Mexico-UNAM, Mexico City 04510, Mexico., Muciño-Olmos EA; Division of Translational Cancer Research, Department of Laboratory Medicine, Lund University, 22381 Lund, Sweden., Aparicio-Bautista DI; Laboratory of Genomics of Bone Metabolism, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico., Basurto-Islas G; Department of Science and Engineering, University of Guanajuato, Leon 37670, Guanajuato, Mexico., Baltiérrez-Hoyos R; Laboratory of Fibrosis and Cancer, Faculty of Medicine and Surgery, 'Benito Juárez' Autonomous University of Oaxaca-UABJO, Oaxaca 68120, Mexico.; Deputy Directorate of Humanistic and Scientific Research, National Council of Humanities, Sciences and Technologies-CONAHCYT, Mexico City 03940, Mexico., Vásquez-Garzón VR; Laboratory of Fibrosis and Cancer, Faculty of Medicine and Surgery, 'Benito Juárez' Autonomous University of Oaxaca-UABJO, Oaxaca 68120, Mexico.; Deputy Directorate of Humanistic and Scientific Research, National Council of Humanities, Sciences and Technologies-CONAHCYT, Mexico City 03940, Mexico., Villa-Treviño S; Department of Cell Biology, Center for Research and Advanced Studies of the National Polytechnic Institute-CINVESTAV-IPN, Mexico City 07360, Mexico., Muriel P; Laboratory of Experimental Hepatology, Department of Pharmacology, Center for Research and Advanced Studies of the National Polytechnic Institute-CINVESTAV-IPN, Mexico City 07360, Mexico., Serrano H; Department of Health Sciences, Div CBS, Metropolitan Autonomous University-Iztapalapa Campus, Mexico City 09340, Mexico., Pérez-Carreón JI; Laboratory of Liver Diseases, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico., Arellanes-Robledo J; Laboratory of Liver Diseases, National Institute of Genomic Medicine-INMEGEN, Mexico City 14610, Mexico.; Deputy Directorate of Humanistic and Scientific Research, National Council of Humanities, Sciences and Technologies-CONAHCYT, Mexico City 03940, Mexico. |
| Abstrakt: |
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. |
