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This observation indicates that cardiomyocytes triggered self-compensation through reduced exogenous FA uptake and increased intracellular metabolism in response to excessive lipids in the cytoplasm

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CX3CR1 / mice show more extensive neuronal degeneration than littermate controls, which is associated with microglia dysregulation, and studies with these mice confirmed the neuroprotective role of the CX3CL1/CX3CR1 interaction [120]