ReviewAmerican journal of cardiovascular disease2025
Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.
Review in American journal of cardiovascular disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Optimal Duration of Ultrasound-Facilitated Catheter-Directed Thrombolysis for Acute Pulmonary Embolism: A Retrospective Cohort Study.Biomedicines · 2026Article
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Dose- and time-dependent cardioprotection of liproxstatin-1 via sequential modulation of ferroptosis pathways after myocardial ischemia-reperfusion.Molecular and cellular biochemistry · 2026Article
- Kaempferol Attenuates Myocardial Ischemia-Reperfusion Injury by Suppressing Ferroptosis via the KEAP1-Nrf2-GPX4 Axis.The Kaohsiung journal of medical sciences · 2026Article
- The Mechanism of G Protein-Coupled Receptor Regulation of Ferroptosis in Hepatic Ischemia-Reperfusion Injury.International journal of molecular sciences · 2026Review
- Ferroptosis, lipid metabolism, and genetic regulation in postoperative rehabilitation of elderly hip fractures: from molecular mechanisms to clinical translation.Frontiers in genetics · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis is a novel form of programmed cell death characterized by iron-dependent lipid peroxidation (LPO). It has been widely demonstrated in the last years to play a crucial pathogenic role in ischemia-reperfusion injury (IRI). The pathological basis for ferroptosis is established through disturbances in energy metabolism, iron homeostasis and mitochondrial injury during ischemic phase. During the following period of reperfusion, the surge in reactive oxygen species (ROS), along with the liberation of inflammatory mediators, and the aggravation of LPO, will further stimulate peroxidase 4 (GPX4) inactivation and augment iron load in the cells, which will greatly intensify bodily tissue injury. Ferroptosis, which operates through intricate cross-regulation with oxidative stress, immune-inflammatory responses, and autophagy, forms a multi-tiered positive feedback loop that actively contributes to injury-repair imbalance IRI pathogenesis across various organs, including the heart, brain, liver and kidney. Studies show that tissue damage and recovery can be improved by targeting system Xc
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