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TNF- damages cardiomyocyte mitochondria by inhibiting glycolysis and reducing mitochondrial adenosine triphosphate (ATP) production through promoting oxidative and nitrosative stress, which can result in compromised cardiac systolic function and unfavorable cardiac remodeling [83, 84]

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The combined electrophysiological analysis further shows an overall reduction in functional expression of NR2A subunits along with relative increases in both, contribution of NR2B to the synaptic and extrasynaptic NMDAR-mediated currents and the magnitude of extrasynaptic NMDAR-mediated currents in lesioned HMNs

Anchor logic: why the two are stacked Think of tissue repair as a construction project with two independent bottlenecks