Fig. 2: The degeneracy of the damage sensor triggers inflammaging.
From: Age-related cerebral small vessel disease and inflammaging
Exogenous and endogenous danger stimuli interact with pattern recognition receptors (PRRs) expressed on the cell surface and in the cytoplasm. Danger molecules can be non-self (pathogen-associated molecular patterns, PAMPs), self (damage-associated molecular patterns, DAMPs) and quasi-self (nutritional and metabolic products from the gut microbiota). These multitude of stimuli converge on the same evolutionarily selected promiscuous sensors, and trigger inflammaging.
