Mixed
Cellular senescence drives inflammaging through the secretion of the Senescence-Associated Secretory Phenotype (SASP), which promotes chronic sterile inflammation and age-related pathologies.
Aging is associated with the accumulation of 'zombie' cells (senescent cells) that secrete inflammatory signals (SASP). This chronic inflammation contributes to many age-related diseases. While senolytics (drugs that kill these cells) are being developed, current evidence supports lifestyle factors like physical activity, which improves mitochondrial function and may help manage inflammation.
Senescent cells and the senescence-associated secretory phenotype (SASP), now widely acknowledged as drivers of aging and age-related diseases, have emerged as key players in inflammaging.
Why this rating
Supported by extensive preclinical models and emerging human proteomic/omics data, though human trials are still early.
Source
Connecting aging biology and inflammation in the omics era
Keenan A. Walker et al. · Journal of Clinical Investigation · 2022
DOI 10.1172/jci158448
More from this paper
- Multi-omics approaches (proteomics, transcriptomics) are necessary to accurately measure and understand the complexity of inflammaging, as single biomarkers like IL-6 or TNF-α are insufficient.Strong
- Mitochondrial dysfunction, specifically the release of mitochondrial DAMPs (mtDAMPs) like oxidized mtDNA and cardiolipin, activates innate immune pathways (NLRP3, cGAS/STING, NF-κB) to drive inflammaging.Good
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