Furthermore, analysis of key genes within the enriched pathways showed a trend toward corrected expression of markers related to cardiac hypertrophy, fibrosis, inflammation, and mitochondrial respiration following AAV-BCKDK treatment in OCM mice ( Fig. 5 F).
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BCKDK protects against obesity-induced cardiac remodelling and dysfunction by alleviating mitochondrial oxidative stress and ROS-driven MAPK signalling.
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