In the cardiac hypertrophy induced by high fructose, CFTR expression decreased and CFTR silencing resulted in mitochondrial oxidative stress [158], whereas in intestinal epithelial cells, CFTR deletion resulted in lipid homeostasis disruption and mitochondrial changes such as reduced cytochrome c level, lowered expression of OXPHOS complexes and a high ADP/ATP ratio [159,160]. Here, CFTR is linked to cardiac hypertrophy.