fig2
Figure 2. TAFAZZIN knockdown in neonatal cardiac fibroblasts. Knockdown of the TAFAZZIN gene disrupts mitochondrial homeostasis and alters mitochondrial membrane structure, leading to slightly reduced ATP levels and increased AMP concentrations. This schematic is adapted primarily from the work of He et al.[51] and reproduced with permission from American Journal of Physiology, Heart and Circulatory Physiology, courtesy of the American Physiological Society, USA. Elements have also been adapted from Ref.9[9], with permission from Frontiers in Genetics. ATP: adenosine triphosphate; AMP: adenosine monophosphate.