I discuss the complex but potent interactions of TLR signaling with plasma membrane protein complexes including semaphorin cytoplasmic kinase interactions leading to PPAR gamma transcription that fires off CD36 and beta oxidation gene transcription to switch M1 to M2 macrophage polarity thus feedback regulating the pro-inflammatory glycolytic mToRC system dynamics.
Aging is associated with a corruption in this fine-tuning that presents in the older sedentary human individual as a simple dysregulation of inflammation that ultimately impairs the ability to ward off otherwise relatively innocuous pathogens while simultaneously punctuating the equilibrium otherwise exerted to control tissue repair and the potential for cellular proliferation and oncogenesis.
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