Ferroptosis: Mechanisms and Roles in Diseases

Dear Colleagues,

We are pleased to invite you to contribute to this Special Issue on “Ferroptosis: Mechanisms and Roles in Diseases”. Ferroptosis is a distinct form of regulated cell death characterized by iron-dependent lipid peroxidation and collapse of redox homeostasis. Since its identification, ferroptosis has emerged as a critical mechanism in a wide range of pathological processes, including metabolic dysfunction, endocrine-related disorders, inflammation, tissue injury, neurodegeneration, cardiovascular disease, cancer, and aging.

Increasing evidence indicates that ferroptosis is closely linked to key biological processes highly relevant to endocrinology and metabolism, such as iron handling, lipid metabolism, mitochondrial dysfunction, oxidative stress, antioxidant defense, and hormone-responsive signaling pathways. Dysregulated ferroptotic responses may contribute to the development and progression of obesity, diabetes, metabolic syndrome, metabolic dysfunction-associated fatty liver disease, thyroid disorders, reproductive dysfunction, osteoporosis, and other endocrine- and metabolism-related conditions.

Moreover, ferroptosis is increasingly recognized as a mechanistic interface through which environmental exposures and behavioral factors may influence disease risk. External factors such as air pollution, heavy metals, endocrine-disrupting chemicals, and temperature-related stress, together with modifiable behaviors including diet, physical activity, sleep, sedentary lifestyle, and circadian disruption, may alter iron metabolism, redox balance, and lipid peroxidation, thereby modulating ferroptosis susceptibility and disease outcomes. A deeper understanding of ferroptosis from molecular, physiological, clinical, and population perspectives may therefore provide important opportunities for mechanistic discovery, risk assessment, and therapeutic innovation.

This Special Issue aims to gather original research articles and comprehensive reviews addressing the molecular mechanisms, biological functions, and pathological significance of ferroptosis in disease. Particular emphasis will be placed on studies that clarify how ferroptosis is initiated, regulated, and integrated with broader disease processes, especially in endocrine and metabolic tissues and disorders.

The topic is closely aligned with the scope of Molecular Endocrinology and Metabolism, as ferroptosis intersects with many central themes of the journal, including endocrine systems and endocrine-related diseases, molecular and cellular mechanisms, pathophysiology, metabolism, obesity, diabetes, reproductive disease, osteoporosis, aging, inflammation, oxidative stress, and endocrine disruption. In addition to fundamental mechanistic studies, this Special Issue also welcomes interdisciplinary research exploring how environmental exposures and health-related behaviors shape ferroptosis-related pathways and contribute to disease susceptibility, progression, and intervention responses.

By bringing together mechanistic, translational, and clinically relevant studies, this collection seeks to advance understanding of ferroptosis in disease etiology and support the development of new biomarkers, preventive strategies, and therapeutic approaches.

In this Special Issue, original research articles and reviews are welcome. Research areas may include, but are not limited to, the following:

• Molecular and cellular mechanisms of ferroptosis, including iron metabolism, lipid peroxidation, antioxidant defense systems, mitochondrial dysfunction, and redox signaling;
• Ferroptosis in endocrine and metabolic disorders, including obesity, diabetes, metabolic syndrome, metabolic liver disease, thyroid disease, adrenal disorders, pituitary dysfunction, reproductive disorders, and osteoporosis;
• Crosstalk between ferroptosis and related pathways, such as inflammation, oxidative stress, autophagy, apoptosis, necroptosis, senescence, and hormonal signaling;
• Environmental determinants of ferroptosis, including air pollution, heavy metals, endocrine-disrupting chemicals, temperature-related stress, and other external exposures;
• Behavioral and lifestyle modulators of ferroptosis, including diet, nutrient status, physical activity, sleep, sedentary behavior, and circadian rhythm disruption;
• Genetic, epigenetic, transcriptomic, proteomic, and metabolomic studies of ferroptosis-related pathways in disease;
• Biomarkers, experimental models, and methodological advances for detecting and quantifying ferroptosis in biological systems;
• Population-based, clinical, and translational studies evaluating the relevance of ferroptosis to disease prevention, prognosis, and therapy;
• Pharmacological, nutritional, and environmental interventions targeting ferroptosis in disease treatment and management.

We look forward to receiving your contributions.

Dr. Yuquan Chen
Guest Editor

Manuscript Submission Information

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