Regulated Cell Death and Disease
Submission Deadline: 30 Jun 2025
Guest Editors

Department of Geriatrics, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China
Interests: regulated cell death; ferroptosis; cuproptosis; pyroptosis; Alzheimer's disease; Parkinson's disease; neuroprotection; neuropharmacology; epigenetic modification

Division of Neurobiology, Johns Hopkins University, Baltimore, MD, USA
Interests: neuropharmacology; early parkinsonism; sleep regulation; neuroimmunology; glymphatic system; Huntington’s disease; Alzheimer's disease; Parkinson's disease; neuroprotection

Department of Respiratory and Critical Care Medicine, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China
Interests: cancer; regulated cell death; ferroptosis; cuproptosis; cancer drug resistance
Special Issue Information
Dear Colleagues,
During the past two decades, research has uncovered several forms of regulated cell death (RCD), which include necroptosis, pyroptosis, parthanatos, ferroptosis, cuproptosis, lysozincrosis, and disulfidptosis. RCD is critical for the development and homeostasis of almost all multicellular organisms. Dysregulation of RCD leads to diverse disease states. However, knowledge of the role of RCD in different diseases is still in its infancy. It is crucial to determine the detailed mechanisms by which various types of RCD play a role in the pathogenesis of diseases. Accumulating evidence supports the pharmacological modulation of RCD as a therapeutic target for diseases.
The aims of this research topic are:
(1) To delineate the role of RCD in various diseases, including cancers and non-cancerous diseases.
(2) To uncover novel therapy regimens by targeting RCD.
We welcome submissions of original research, reviews, mini-reviews, and systematic reviews that explore a wide range of topics that include, but are not limited to, the following:
- How dysregulation of RCD leads to pathogenesis of diseases
- How epigenetic and post-translational modifications regulate RCD to cause diseases
- How the interplay of different types of RCD contribute to diseases
- How the interplay of cell signaling pathways, such as cGAS-STING, in different RCDs, contribute to diseases
- Strategies for targeting RCD to treat diseases
Prof. Hongquan Wang, Lida Du and Yumin Wang
Guest Editors
Keywords
- cell death
- ferroptosis
- pyroptosis
Manuscript Submission Information
Manuscripts should be submitted via our online editorial system at https://imr.propub.com by registering and logging in to this website. Once you are registered, click here to start your submission. Manuscripts can be submitted now or up until the deadline. All papers will go through peer-review process. Accepted papers will be published in the journal (as soon as accepted) and meanwhile listed together on the special issue website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts will be thoroughly refereed through a double-blind peer-review process. Please visit the Instruction for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted manuscripts should be well formatted in good English.
Published Papers (3)
Ferroptosis in Neurovascular Unit of Ischemic Stroke: Multidimensional Regulatory Mechanisms and Targeted Interventions
Front. Biosci. (Landmark Ed) 2025, 30(11), 40737; https://doi.org/10.31083/FBL40737
(This article belongs to the Special Issue Regulated Cell Death and Disease)
HOTAIR Knockdown Increases the Sensitivity of Hepatocellular Carcinoma Cells to Sorafenib by Disrupting miR-145-5p/HK2 Axis-Mediated Mitochondrial Function and Glycolysis
Front. Biosci. (Landmark Ed) 2025, 30(5), 37368; https://doi.org/10.31083/FBL37368
(This article belongs to the Special Issue Regulated Cell Death and Disease)
Leukemia Inhibitory Factor Attenuates Hypoxic–Ischemic White Matter Injury via NLRP3 Inflammasome Activity Suppressing Through the Nrf2/HO-1 Pathway
Front. Biosci. (Landmark Ed) 2025, 30(3), 36630; https://doi.org/10.31083/FBL36630
(This article belongs to the Special Issue Regulated Cell Death and Disease)
