PhD Scientific Days 2026

Molecular Medicine 4.

Investigating Ferroptosis and Autophagy Interactions through Integrated Database Analysis

Előadó neve

Bence, Hajdú, PhD

Előadó munkahelye

Department of molecular Biology

Szerző(k) neve és munkahelye

Bence Hajdú¹

1: Department of molecular Biology

Összefoglaló szövege

Ferroptosis is an iron-dependent, regulated form of cell death characterized by peroxidation
of polyunsaturated fatty acids (PUFAs), reactive oxygen species (ROS) accumulation, and
loss of redox homeostasis. Two pathways of ferroptosis have been identified: an extrinsic
pathway characterized by increased iron uptake and decreased cysteine/glutamate uptake,
and an intrinsic pathway involving the inhibition of glutathione peroxidase 4 (GPX4), a crucial
antagonist of ferroptosis that maintains redox homeostasis.
Ferroptosis has been implicated in several diseases, including neurodegeneration and
inflammatory bowel disease (IBD). A growing body of evidence suggests a complex interplay
between ferroptosis and another cell death mechanism, autophagy. An increasing number of
studies suggest that the two processes are not independent. However, whether they have a
positive or negative effect on each other remains unclear.
To elucidate these connections, we developed an integrated, ferroptosis-specific interaction
database, FerroNet. This was achieved by programmatically compiling data from multiple
existing sources. The resultant graph database features a schema compatible with the
AutophagyNet database, facilitating direct pathway analysis and comparison between
ferroptosis and autophagy. FerroNetincludes ferroptosis-related protein-protein interactions
as well as cell-specific annotations for these interactions. This integrated platform is well-
positioned to identify key regulatory nodes and molecular links between ferroptosis and
autophagy. We assume that it will provide valuable insights into their crosstalk and highlight
potential therapeutic targets.