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NRF1-mediated innate immune response drives inflammaging.

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Nuclear respiratory factor 1 (NRF1) drives cellular senescence and inflammation. Inhibiting NRF1 delays aging and extends lifespan by suppressing innate immune responses, offering potential therapeutic strategies for inflammaging.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Aging Research

Background:

  • Aberrant innate immune responses are linked to cellular senescence.
  • The specific mechanisms connecting innate immunity and senescence are not fully understood.

Purpose of the Study:

  • To investigate the role of nuclear respiratory factor 1 (NRF1) in regulating innate immunity and cellular senescence.
  • To explore NRF1's impact on the senescence-associated secretory phenotype (SASP) and age-related decline.

Main Methods:

  • Studied NRF1's role in senescence induction and SASP regulation.
  • Investigated the NRF1-TBK1/IRF3 pathway and its connection to type I interferon signaling.
  • Utilized NRF1 knockdown in aged mice to assess therapeutic potential.

Main Results:

  • NRF1 deficiency delayed cellular senescence and ameliorated age-related deterioration.
  • NRF1 enhances SASP by regulating TBK1 and IRF3, key innate immunity components.
  • DNA damage-induced ATM kinase phosphorylation of NRF1 exacerbates senescence via the type I interferon axis.
  • NRF1 knockdown mitigated aging phenotypes and extended lifespan in aged mice.

Conclusions:

  • The ATM-NRF1-TBK1/IRF3-type I interferon axis is crucial for DNA damage-induced senescence.
  • Targeting NRF1 presents a promising therapeutic avenue for combating inflammaging and age-related diseases.