PhD Scientific Days 2026

Molecular Medicine 4.

Investigating Ferroptosis and Autophagy Interactions through Integrated Database Analysis

Name of the presenter

Hajdú, Bence

Institute/workplace of the presenter

Department of molecular Biology

Authors

Bence Hajdú¹
1: Department of molecular Biology

Text of the abstract

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.