review · Autophagy
Autophagy is a complex degradation process within cells that exhibits dual functions in survival and death, modulated by cell type and environmental stress. Ferroptosis represents an iron-dependent form of oxidative cell death driven by uncontrolled lipid peroxidation. Specific selective types of autophagy, including ferritinophagy, lipophagy, and clockophagy, can initiate or execute ferroptosis by selectively degrading protective proteins or organelles. In contrast, other forms such as reticulophagy and lysophagy bolster cellular defences against ferroptotic damage. Dysregulated autophagy-dependent ferroptosis is linked to a broad range of pathological conditions. To standardise research across the field, an updated definition of autophagy-dependent ferroptosis is provided alongside an overview of key substrates and receptors. The work details experimental methods and establishes consensus guidelines for interpreting data in this evolving area of cell death research.
Cell death mechanisms are fundamental to understanding many severe diseases, but complex overlaps between pathways can cause conflicting research findings. By clarifying how cellular recycling processes promote or block iron-driven cell death, standard guidelines help biomedical researchers reliably detect these events. This consistency accelerates basic discovery by ensuring that laboratories worldwide use comparable definitions and robust experimental methods.
This work represents early-stage foundational research providing experimental guidelines rather than a commercial asset. It may directly assist translational researchers and drug discovery teams in biotechnology or pharmaceutical organisations who need reliable assays to measure cell death targets. Because the material focuses strictly on definitions, detection protocols, and analytical interpretation, practical therapeutic or diagnostic applications remain at a pre-clinical, early research distance from commercial use.
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Macroautophagy/autophagy is a complex degradation process with a dual role in cell death that is influenced by the cell types that are involved and the stressors they are exposed to. Ferroptosis is an iron-dependent oxidative form of cell death characterized by unrestricted lipid peroxidation in the context of heterogeneous and plastic mechanisms. Recent studies have shed light on the involvement of specific types of autophagy (e.g. ferritinophagy, lipophagy, and clockophagy) in initiating or executing ferroptotic cell death through the selective degradation of anti-injury proteins or organelles. Conversely, other forms of selective autophagy (e.g. reticulophagy and lysophagy) enhance the cellular defense against ferroptotic damage. Dysregulated autophagy-dependent ferroptosis has implications for a diverse range of pathological conditions. This review aims to present an updated definition of autophagy-dependent ferroptosis, discuss influential substrates and receptors, outline experimental methods, and propose guidelines for interpreting the results.<b>Abbreviation</b>: 3-MA:3-methyladenine; 4HNE: 4-hydroxynonenal; ACD: accidentalcell death; ADF: autophagy-dependentferroptosis; ARE: antioxidant response element; BH2:dihydrobiopterin; BH4: tetrahydrobiopterin; BMDMs: bonemarrow-derived macrophages; CMA: chaperone-mediated autophagy; CQ:chloroquine; DAMPs: danger/damage-associated molecular patterns; EMT,epithelial-mesenchymal transition; EPR: electronparamagnetic resonance; ER, endoplasmic reticulum; FRET: Försterresonance energy transfer; GFP: green fluorescent protein;GSH: glutathione;IF: immunofluorescence; IHC: immunohistochemistry; IOP, intraocularpressure; IRI: ischemia-reperfusion injury; LAA: linoleamide alkyne;MDA: malondialdehyde; PGSK: Phen Green™ SK;RCD: regulatedcell death; PUFAs: polyunsaturated fatty acids; RFP: red fluorescentprotein;ROS: reactive oxygen species; TBA: thiobarbituricacid; TBARS: thiobarbituric acid reactive substances; TEM:transmission electron microscopy.
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DOI: 10.1080/15548627.2024.2319901
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