Restoration of autophagy regulation
Intracellular proteotoxicity of toxic and pro-inflammatory advanced glycation end products (AGEs) is restricted by two main proteolytic pathways: ubiquitin-proteasome system (UPS) and autophagy. Autophagy is the main pathway for the degradation of cytosolic, aggregated, or insoluble proteins and organelles that cannot be disposed through the proteasome. The function of these pathway declines with age. As a result, protein aggregates and non-functional organelles accumulate in old tissues. Advanced glycation end products contribute to an increase in the rigidity of the extracellular matrix with age. This is one of the underestimated signs of aging leading to fibrosis, mitochondrial dysfunction and epigenetic changes.
We aim to search for target genes, creating a platform for treatment development to restore the autophagy regulation.