Novel Mechanisms and Therapeutic Opportunities of Ferroptosis

Dear Colleagues,

Ferroptosis is a newly identified regulated cell death modality with unique characteristics compared to apoptosis and other types of cell death. Ferroptosis is caused by the disruption of several key metabolic pathways (including the ROS, amino acid, and lipid metabolism pathways) in the cell and is dependent on iron. There are three basic elements for ferroptosis: the substrate of lipid peroxidation, the executor of lipid peroxidation, and the anti-ferroptosis system.

The past decade witnessed the rapid progress in ferroptosis research, both in terms of its molecular mechanism and disease relevance. Classical models of ferroptosis highlight the central role of ACSL4 in the synthesis of the lipid peroxidation substrate, ALOXs as executors of lipid peroxidation, and GPX4 for ferroptosis suppression. Ferroptosis has been demonstrated to be involved in normal development and diverse disorders, including ischemic organ injuries, neurodegenerative diseases, immune system activities, and tumors. The pathological relevance of ferroptosis provides new therapeutic opportunities for these diseases.

As research on ferroptosis goes deeper, novel mechanisms of ferroptosis that are beyond the classical model are emerging. For example, p53-mediated ferroptosis has been proven to be as much of a distinct pathway as GPX4-centered ferroptosis. More and more regulators of ferroptosis are being identified. In addition, ferroptosis exhibits many more roles than expected in the initiation and development of various diseases. More efforts should be made to determine the novel mechanisms and therapeutic opportunities of ferroptosis.

This Special Issue aims to collect papers about how ferroptosis is regulated and how ferroptosis pathways can be targeted to treat diverse diseases. We welcome papers about novel/non-canonical ferroptosis pathways and new drugs therapeutic methods targeting ferroptosis.

Original research articles, reviews, and mini-reviews are welcome in this collection. Topics of interest include but are not limited to the follow:

1. Novel mechanisms and regulators of ferroptosis;
2. The role of p53 in both canonical and non-canonical ferroptosis regulation;
3. Targeting ferroptosis for the treatment of various diseases.

Please note that the findings based on bioinformatic data mining should be validated by experiments.

Dr. Yanqing Liu
Dr. Zhenyi Su
Prof. Dr. Chaoyun Pan
Prof. Dr. Lianxiang Luo
Dr. Xin Wang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.