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Metabolism, long perceived as mere supplier of ATP, is increasingly appreciated to reflect and determine cellular phenotypes

Ultimately, it seems as though injury to the NMJ is a culmination of mutant protein aggregation at the presynaptic nerve terminal, presynaptic cholinergic dysfunction, impaired axonal transport, reduced synaptic acetylcholinesterase, and diseased muscle itself, among others [292]

Endometrial cells account for the increased number of peritoneal macrophages by producing monocyte chemoattractant protein (MCP)-1 and IL-6 (45)

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