Divine Aleru, Microbiome Medicine Research Coordinator

This study shows that gut microbiota–derived short-chain fatty acids can reduce erastin-induced lipid peroxidation and modulate iron and ATF3 signaling in cardiomyocytes. The findings link microbial metabolites to ferroptosis control during ischemic-like stress in heart cells.

This review connects gut microbiota dysbiosis to ferroptosis biology in chronic kidney disease, emphasizing how microbial metabolites and altered antioxidant defenses can amplify iron-driven lipid peroxidation. It highlights functional shifts toward fewer SCFA producers and more uremic toxin producers and discusses diet and microbial interventions.

This review explains how ferroptosis drives tubular injury in acute kidney injury through iron overload and lipid peroxidation. It connects key regulators like system Xc−, GPX4, Nrf2, and ACSL4 to AKI models and highlights drug strategies that block ferroptosis.

This review explains how ferroptosis drives lipid peroxidation and brain injury in ischemic and hemorrhagic stroke. It summarizes drug targets and inhibitors such as ferrostatin-1, liproxstatin-1, selenium/GPX4 support, N-acetylcysteine, and iron chelation, and it discusses translation limits.

This study shows that GPX4 protects neurons by anchoring to membranes through a hydrophobic fin-loop. A patient R152H mutation collapses this loop, triggers ferroptosis in patient neurons and organoids, and drives Alzheimer’s-like brain signatures in mice.

This review connects Alzheimer’s neurodegeneration to ferroptosis, an iron-driven, lipid-peroxidation cell-death program. It summarizes human and model evidence linking brain iron, GPX4 antioxidant defense failure, and amyloid/tau-related iron handling to cognitive decline, and outlines therapy angles that target iron–redox stress.

This review links ferroptosis to Alzheimer’s and Parkinson’s disease by connecting iron imbalance, mitochondrial stress, and lipid peroxidation to neuronal loss. It highlights LOX-driven oxidized phospholipids, ACSL4-dependent lipid vulnerability, VDAC2-related iron handling, and ferritinophagy as key mechanisms, and it prioritizes Nrf2/Bach1 as actionable therapeutic targets.

This study shows that T-cell stimulation lowers GPX4 protection and shifts activated T cells toward ferroptosis. Ferroptosis vulnerability varies by subset and tracks with GPX4 expression. GPX4 inhibition weakens CAR-T killing and cytokine output, while ferroptosis inhibition restores function and improves antitumor activity.

This review explains how ferroptosis shapes tumor immunity. Tumor ferroptosis can boost antigen presentation and T-cell killing, but ferroptosis in immune cells weakens surveillance and therapy response. Key control points include GPX4, system Xc−, iron handling, and lipid peroxidation.

This review explored the role of selenium in ferroptosis, focusing on its essential involvement through glutathione peroxidase 4 (GPX4), a key selenoenzyme that protects against lipid peroxidation and ferroptosis. It examines the dual role of selenium in regulating iron-dependent lipid peroxidation and the mechanisms through which selenium, via GPX4 and other selenoproteins, […]

This study demonstrates that GPX4 is essential for motor neuron survival, with its ablation in mice leading to rapid motor neuron degeneration and paralysis via ferroptosis. Vitamin E supplementation delays disease onset, highlighting the potential for ferroptosis inhibition in treating neurodegenerative diseases.

This study identifies GPX4 as essential for human erythroblast enucleation, independent of ferroptosis. The results show that lipid raft clustering and myosin phosphorylation, which are necessary for enucleation, are disrupted in GPX4-deficient cells, and cholesterol supplementation can partially restore enucleation efficiency.

The research paper reviewed the roles of GPX4 (Glutathione Peroxidase 4) in cell death, particularly focusing on its function in ferroptosis, autophagy, and disease. GPX4, a key selenoenzyme, plays a pivotal role in mitigating lipid peroxidation, thus protecting cells from oxidative stress and various forms of regulated cell death (RCD). The study […]

This review explains why stopping membrane lipid peroxidation is the most reliable way to block ferroptosis. It compares endogenous defenses with synthetic inhibitors and shows that optimized radical-trapping antioxidants offer the strongest in vivo potential, while many upstream strategies remain less consistent across models.

This review explains how a gut bacterial tryptophan metabolite, IDA, can promote colorectal cancer by blocking ferroptosis through an AHR–ALDH1A3–FSP1–CoQ10 pathway. It reframes microbial metabolites as direct regulators of tumor cell death vulnerability, not just immune modifiers.

This was an experimental mechanistic study that tested whether GPX4 is a central regulator of ferroptosis and whether chemically inducing GPX4 failure can selectively kill cancer cells and suppress tumor growth. The authors compared multiple ferroptosis-inducing small molecules and used metabolomics, chemoproteomics, and genetic modulation to map where these compounds converge. They […]

This review explains how ferroptosis, driven by iron dysregulation and lipid peroxidation, exacerbates neuronal injury in ischemic stroke. It evaluates therapeutic strategies like ferrostatin-1, liproxstatin-1, and iron chelation, highlighting FABP5 as a potential biomarker for monitoring ferroptosis in stroke.

This review explains how ferroptosis drives kidney injury through iron-dependent lipid peroxidation when GPX4- and FSP1-based defenses fail. It highlights proximal tubule vulnerability, links ferroptosis to ischemia–reperfusion and nephrotoxins, and summarizes anti-ferroptotic strategies that protect kidneys in models.

This review explains how lipid metabolism drives ferroptosis by shaping oxidation-prone membrane phospholipids and controlling iron-dependent lipid peroxidation. It highlights ACSL4 and LPCAT3 remodeling, GPX4 and system xc− defenses, and backup antioxidant pathways such as FSP1–CoQ10 and GCH1–BH4, with implications for cancer and tissue injury.

This review explains how ACSL enzymes reshape tumor fatty-acid use and control ferroptosis and cancer immunity. It contrasts ACSL4-driven polyunsaturated lipid remodeling that promotes ferroptosis with ACSL3-oleic acid programs that resist ferroptosis, and it links these pathways to immunotherapy response.

This review explains ferroptosis, an iron-driven, lipid peroxidation cell-death pathway linked to metabolism and redox balance. It highlights key control points such as system xc−, glutathione, GPX4, lipid remodeling, and iron handling, and it connects these mechanisms to cancer and tissue injury.

This paper reviewed ferroptosis as a regulated, non-apoptotic form of cell death driven by iron-dependent lipid peroxidation, then mapped the main molecular “pressure points” that determine whether cells resist or enter ferroptosis. It focused on core chemistry (iron handling and lipid oxidation), the best-supported defense systems that stop membrane damage, and how […]

This study defined and experimentally mapped a distinct form of regulated cell death that the authors named ferroptosis. They used the RAS-selective small molecule erastin to trigger this phenotype, then tested what conditions were required for death, what cellular damage accumulated first, and how this process differed from apoptosis, necrosis, and autophagy. […]

Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by social, communication, and behavioral challenges. It involves genetic and environmental factors, including microbiome imbalances which influence symptom severity and overall health.