Ferroptosis is described as an iron-linked programmed cell death process associated with ROS formation and lipid peroxidation.
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ferroptosis
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Ferroptosis as a Novel Therapeutic Strategy to Overcome Multidrug Resistance in Colorectal Cancer
FGF–FGFR Signaling in Parkinson’s Disease: Mechanistic Links to Ferroptosis and Neuroprotection
Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, has emerged as a critical player in MM pathology and treatment.
Reactive Oxygen Species Across Death Pathways: Gatekeepers of Apoptosis, Ferroptosis, Pyroptosis, Paraptosis, and Beyond.
dysregulation of intracellular iron homeostasis produces excessive reactive oxygen species (ROS) via the Fenton reaction and causes devastating effects on cells, leading to ferroptosis, an iron-dependent cell death
Recent studies revealed that SLC7A11 overexpression promotes tumor growth partly through suppressing ferroptosis, a form of regulated cell death induced by excessive lipid peroxidation.
The review title explicitly names ferroptosis as the central topic.
ferritinophagy, which can release sufficient iron to initiate the unique programmed cell death process ferroptosis causing ROS formation and lipid peroxidation
The supplied web research summary states that the 2018 NCCD recommendations explicitly cover ferroptosis.
Supporting Sources
Source 1primary paper2026PMC
Source 2primary paper2026PMC
Linked Claims
The paper presents ferroptosis as a therapeutic strategy to overcome multidrug resistance in colorectal cancer.
Quoted textsource-backed
Ferroptosis as a Novel Therapeutic Strategy to Overcome Multidrug Resistance in Colorectal Cancer
The paper addresses FGF–FGFR signaling in Parkinson’s disease in relation to mechanistic links to ferroptosis and neuroprotection.
The review summarizes anti-myeloma ferroptosis modulation mechanisms as lipid metabolism reprogramming, ferritinophagy-driven iron homeostasis regulation, ROS-mediated oxidative stress potentiation, autophagic activation, and genes and proteins regulation.
Quoted textsource-backed
mechanistically mediated through: 1) lipid metabolism reprogramming; 2) ferritinophagy-driven iron homeostasis regulation; 3) Reactive oxygen species (ROS)-mediated oxidative stress potentiation; 4) autophagic activation; 5) Genes and proteins regulation.
Ferroptosis is a critical player in multiple myeloma pathology and treatment.
Quoted textsource-backed
Ferroptosis, a form of cell death driven by iron-dependent lipid peroxidation, has emerged as a critical player in MM pathology and treatment.
The review recommends prioritizing development of biomarkers and ferroptosis inducers to advance ferroptosis-targeting anticancer compounds for multiple myeloma.
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Prioritize developing biomarkers and ferroptosis inducers to advance novel ferroptosis-targeting anticancer compounds.
Natural products and certain antitumor compounds exert anti-multiple myeloma effects via modulation of ferroptosis-related pathways.
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NPs and antitumor compounds exert anti-MM effects via ferroptosis modulation
Clinical translation of ferroptosis-modulating natural products and antitumor compounds in multiple myeloma is hindered by single-target mechanistic focus without systems pharmacology-level network analysis and by overreliance on in vitro models with insufficient clinical validation.
Quoted textsource-backed
clinical translation faces two critical hurdles: 1) predominant focus on single-target mechanisms lacking systems pharmacology-level network analysis; 2) overreliance on in vitro models with insufficient clinical validation.
The review states that 4-HNE, described as an end-product of ferroptosis, promotes inflammatory responses associated with amyloid-beta fibrils and neurofibrillary tangles in Alzheimer's disease and alpha-synuclein aggregation in Parkinson's disease.
The review concludes that intracellular iron homeostasis is vital for maintaining inflammatory homeostasis.
Dysregulation of intracellular iron homeostasis produces excessive ROS via the Fenton reaction and can lead to ferroptosis.
SLC7A11 overexpression promotes tumor growth partly by suppressing ferroptosis.
FerrDb is a curated resource relevant for ferroptosis regulator, marker, and disease-association mapping.
This source is a broad review of ferroptosis covering its past, present, and future.
Ferritinophagy can release enough iron to initiate ferroptosis, but inclusion body buildup in hereditary ferritinopathy suggests suppressed ferritinophagy together with iron leakage and ROS stress may produce a long-term ferroptotic-like state.
This NCCD 2018 recommendations review covers multiple major cell-death modalities including apoptosis, MPT-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, and immunogenic cell death.
Quoted textsource-backed
Anchor article: the 2018 Nomenclature Committee on Cell Death (NCCD) recommendations is a broad consensus review that explicitly covers major regulated cell death modalities including intrinsic/extrinsic apoptosis, MPT-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, and immunogenic cell death.