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Activation of the classical complement pathway is initiated by C1qs recognition of specific molecules on the surface of apoptotic or stressed cells, such as calreticulin, which serves as a canonical eat-me signal that facilitates C1q binding (115)
The inhibition of miR-155 rescues redox homeostasis and mitochondrial dynamics in diabetic tissues via AMPK-PGC1 signaling (Prieto et al., 2023
TREM2 sustains microglial expansion during aging and response to demyelination
When that balance is strained, tissues may feel more reactive and less resilient
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