First-pass extracted concept

senescence-associated secretory phenotype

Candidate: concept label2 source documents4 linked claims

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Aliases

SASP

Evidence Snippets

NRF1 enhanced SASP by transcriptionally regulating TBK1 and IRF3, critical nodes in innate immunity essential for senescence induction.

Evidence 1Source 1DOI PubMedprovenance

RNA viruses such as HCV and HIV induce ROS generation, DNA damage, induction of senescence-associated secretory phenotype (SASP)...

Evidence 2Source 2DOI PubMedprovenance

Supporting Sources

Source 1primary paper2025MEDDOI PubMed

1 evidence snippet 2 linked claims Claim 1 Claim 2

Source 2review2022Frontiers in ImmunologyDOI PubMed

1 evidence snippet 2 linked claims Claim 1 Claim 2

Linked Claims

Claim 1mechanistic regulationsupports2025Source 1DOI PubMed

NRF1 enhances SASP by transcriptionally regulating TBK1 and IRF3.

Quoted textsource-backed

Mechanistically, NRF1 enhanced SASP by transcriptionally regulating TBK1 and IRF3, critical nodes in innate immunity essential for senescence induction.

Claim 2mechanistic rolesupports2025Source 1DOI PubMed

NRF1 orchestrates innate immune responses that drive senescence and SASP.

Quoted textsource-backed

Here, we elucidate the pivotal role of nuclear respiratory factor 1 (NRF1) in orchestrating innate immune responses that drive senescence and the senescence-associated secretory phenotype (SASP).

Claim 3mechanistic summarysupports2022Source 2DOI PubMed

RNA viruses including HCV and HIV are described as inducing ROS generation, DNA damage, SASP, metabolic reprogramming, G1 cell-cycle arrest, telomere shortening, and epigenetic modification.

Claim 4mechanistic summarysupports2022Source 2DOI PubMed

SARS-CoV-2 is described as a potent inducer of cytokine storm and SASP, and its spike protein is described as promoting an endothelial senescence phenotype with increased p16, p21, SA-β-Gal, and adhesion molecules.