Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210 and BSO-Induced Ferroptosis
preprint
OA: closed
CC-BY-4.0
AI-generated summary
This study investigated the proteomic changes in mouse embryonic fibroblasts undergoing ferroptosis induced by erastin, ML210, or BSO.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
Ferroptosis is a unique variety of non-apoptotic cell death, driven by massive lipid oxidation in an iron-dependent manner. Since Ferroptosis was introduced as a concept in 2012, it was shown it's essential role in the pathogenesis in neurodegenerative diseases and an important role in therapy-resistant cancer cells. Thus, a detailed molecular understanding of both canonical and alternative ferroptosis pathways are required. There is a set of widely used chemical agents to modulate ferroptosis using different pathway targets: Erastin blocks cystine-glutamate antiporter, system xc-; ML210 directly inactivate GPX4; L-buthionine sulfoximine (BSO) inhibits γ-glutamylcysteine synthetase, an essential enzyme for glutathione synthesis de novo. Most studies were focused on lipidomic profiling of model systems undergoing death in a ferroptotic modality.
My notes (saved in your browser only)
Citation neighborhood (no data yet)
We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.
Source provenance
- europepmc
- last seen: 2026-05-19T01:45:01.086888+00:00
- unpaywall
- last seen: 2026-08-14T06:25:32.811723+00:00
License: CC-BY-4.0