For example, the overexpression of miR-146a and the knockout of dihydrolipoyl succinyltransferase (DLST) can both lead to the downregulation of tricarboxylic acid cycle efficiency, causing impaired energy production, similar to the mechanism identified in Ang II- and TAC-induced cardiac hypertrophy and in clinical patients, suggesting that miR-146a and its target DLST are important regulators of the metabolic pathways involved in cardiac hypertrophy (Heggermont et al., 2017). Here, DLST is linked to cardiac hypertrophy.