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Overexpression of NNMT in adipose tissue directly correlates with reduced NAD+ availability, impaired mitochondrial function, and diminished cellular energy expenditure

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Increased levels of programmed cell death 5 (PDCD5) subsequently ameliorated progressive fibrosis and cardiac dysfunction by inhibiting histone deacetylase 3 (HDAC3), suggesting that PDCD5 serves as an endogenous negative feedback regulator in progressive cardiac fibrosis [109]