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- W3183677662 endingPage "1906" @default.
- W3183677662 startingPage "1906" @default.
- W3183677662 abstract "Ageing is a complex process, induced by multifaceted interaction of genetic, epigenetic, and environmental factors. It is manifested by a decline in the physiological functions of organisms and associated to the development of age-related chronic diseases and cancer development. It is considered that ageing follows a strictly-regulated program, in which some signaling pathways critically contribute to the establishment and maintenance of the aged state. Chronic inflammation is a major mechanism that promotes the biological ageing process and comorbidity, with the transcription factor NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) as a crucial mediator of inflammatory responses. This, together with the finding that the activation or inhibition of NF-κB can induce or reverse respectively the main features of aged organisms, has brought it under consideration as a key transcription factor that acts as a driver of ageing. In this review, we focused on the data obtained entirely through the generation of knockout and transgenic mouse models of either protein involved in the NF-κB signaling pathway that have provided relevant information about the intricate processes or molecular mechanisms that control ageing. We have reviewed the relationship of NF-κB and premature ageing; the development of cancer associated with ageing and the implication of NF-κB activation in the development of age-related diseases, some of which greatly increase the risk of developing cancer." @default.
- W3183677662 created "2021-08-02" @default.
- W3183677662 creator A5034545312 @default.
- W3183677662 creator A5046372287 @default.
- W3183677662 creator A5064679206 @default.
- W3183677662 creator A5085715898 @default.
- W3183677662 date "2021-07-27" @default.
- W3183677662 modified "2023-10-18" @default.
- W3183677662 title "Role of NF-κB in Ageing and Age-Related Diseases: Lessons from Genetically Modified Mouse Models" @default.
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