fig2

Cellular ATP levels alone do not reliably reflect overall mitochondrial bioenergetics or mitochondrial dysfunction in Barth syndrome

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.

Journal of Translational Genetics and Genomics
ISSN 2578-5281 (Online)
Follow Us

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/