Key result
IGF-1 inhibited starvation-induced cardiac autophagy and cell death by rescuing mitochondrial metabolism and ATP levels via the Akt/mTOR and AMPK/mTOR pathways.
Why the study?
Does IGF-1 prevent starvation-induced cardiac autophagy and cell death in cardiomyocytes and mice?
Population
Cultured neonatal rat cardiomyocytes and live mice (including liver-specific igf1 deletion mice and wild-type)
Comparison
Insulin-like growth factor 1 (IGF-1) vs Absence of IGF-1 or reduced IGF-1 levels
Design
Preclinical
Authors
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Does not support clinical use; extends animal data on IGF-1 autophagy modulation, hypothesis-generating for human translation.
Does IGF-1 prevent starvation-induced cardiac autophagy and cell death in cardiomyocytes and mice?
IGF-1 protects cardiomyocytes from starvation-induced cell death by maintaining mitochondrial metabolism and inhibiting excessive autophagy.
Troncoso et al. (2011) studied Nutritional stress / starvation-induced cardiac autophagy. IGF-1 vs. Nutritional stress without IGF-1 / wild-type mice was evaluated on Autophagy and cell death rates, ATP levels, oxygen consumption. IGF-1 inhibited starvation-induced cardiac autophagy and cell death by rescuing mitochondrial metabolism and ATP levels via the Akt/mTOR and AMPK/mTOR pathways.
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