Aged kidney: can we protect it? Autophagy, mitochondria and mechanisms of ischemic preconditioning

Figures & data

Figure 1. Appearance and progressive increase of mitochondrial heterogeneity in the aged kidney. In the old kidney, the level of active GSK-3 is increased, which leads to higher percentage of the mitochondria with open pores and higher ROS generation. This results in higher number of dysfunctional mitochondria that are poorly eliminated because of ineffective autophagy. Mechanisms for effective mitochondria clearance induced by IPC or by CR are weak in the old kidney, i.g., because of active Akt. As a result, aged kidney contains more “bad” mitochondria, but they cannot be removed as it occurs in young tissue, leading to enrichment of a population with dysfunctional organelles and the formation of the senile phenotype.