Dysregulated cellular redox status during hyperammonemia causes mitochondrial dysfunction and senescence by inhibiting sirtuin‐mediated deacetylation

Perturbed metabolism of ammonia, an endogenous cytotoxin, causes mitochondrial dysfunction, reduced NAD(+)/NADH (redox) ratio, and postmitotic senescence. Sirtuins are NAD(+)‐dependent deacetylases that delay senescence. In multiomics analyses, NAD metabolism and sirtuin pathways are enriched during...

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Detalles Bibliográficos
Autores principales: Mishra, Saurabh, Welch, Nicole, Karthikeyan, Manikandan, Bellar, Annette, Musich, Ryan, Singh, Shashi Shekhar, Zhang, Dongmei, Sekar, Jinendiran, Attaway, Amy H., Chelluboyina, Aruna Kumar, Lorkowski, Shuhui Wang, Roychowdhury, Sanjoy, Li, Ling, Willard, Belinda, Smith, Jonathan D., Hoppel, Charles L., Vachharajani, Vidula, Kumar, Avinash, Dasarathy, Srinivasan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Research Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10352558/
https://www.ncbi.nlm.nih.gov/pubmed/37101412
http://dx.doi.org/10.1111/acel.13852

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10352558/
https://www.ncbi.nlm.nih.gov/pubmed/37101412
http://dx.doi.org/10.1111/acel.13852

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