Ferroptosis inhibitor FXT-001 shows promise in improving liver and lung transplant outcomes by targeting ischemia-reperfusion injury
By
Tom Vanden Berghe1,15,16,17,18 Send email to [email protected]
Summary
This study identifies an early and transient increase of lipid peroxidation in human liver transplants as a key driver of ischemia-reperfusion injury (IRI). The researchers demonstrate that ferroptosis—an iron-dependent form of cell death triggered by disrupted energy and redox homeostasis—plays a central role in organ dysfunction during transplantation. They validate FXT-001, a ferroptosis inhibitor with dual radical and iron-trapping activity, as a therapeutic agent that provides robust protection in preclinical models, including ex situ perfusion of porcine liver and lung grafts. The findings suggest pharmacological ferroptosis inhibition could improve graft function in human liver and lung transplantation.
Source
bskyFerroptosis inhibitor FXT-001 shows promise in improving liver and lung transplant outcomes by targeting ischemia-reperfusion injurycell.comKey quotes
· 5 pulledIschemia-reperfusion injury (IRI) is a major clinical challenge in transplantation, vascular surgeries, myocardial infarction, and stroke.
Disruption of energy and redox homeostasis triggers ferroptosis, a regulated, iron-dependent form of cell death, leading to organ dysfunction.
We identify an early and transient increase of lipid peroxidation in human liver transplants and validate it as a therapeutic target.
FXT-001, a ferroptosis inhibitor with dual radical and iron-trapping activity, provides robust protection in preclinical models.
Veeckmans et al. demonstrate that ischemia-reperfusion injury triggers an early lipid peroxidation wave in human transplants.
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