Core mechanisms of mitochondrial metabolic reprogramming Supplying flexible fuel: metabolic plasticity and therapeutic resistance CRC cells exhibit pronounced metabolic plasticity, enabling dynamic switching between glycolysis and mitochondrial OXPHOS in response to fluctuations in oxygen, glucose, and other metabolic substrates, thereby adopting a hybrid metabolic phenotype [6]
Emerging cross-kingdom evidence indicates that redox-regulated mitochondrial proteostasis and calcium-dependent stress signalling modules identified in plant systems can inform mechanistic hypotheses in mammalian neurodegeneration
Possible mechanisms include -cell dysfunction caused by decreased -cell mass, oxidative and endoplasmic reticulum stress, impaired insulin synthesis possibly involving mTOR downregulation as shown in experimental models, disrupted amino acidsensing pathways, and pancreatic atrophy, fibrosis, and apoptosis [45,46,47,48] These alterations reflect a coordinated metabolic adaptation to sustain glucose availability and vital organ function under nutrient deprivation [49]
Pharmaceuticals 16 (6), 899
