Ferroptosis in the post-transplantation inflammatory response.
Cell Immunol
; 393-394: 104774, 2023.
Article
en En
| MEDLINE
| ID: mdl-37839157
ABSTRACT
Transplantation is a life-saving therapy for patients with end-stage organ disease. Successful outcomes after transplantation require mitigation of the post-transplant inflammatory response, limiting alloreactivity, and prevention of organ rejection. Traditional immunosuppressive regimens aim to dampen the adaptive immune response; however, recent studies have shown the feasibility and efficacy of targeting the innate immune response. Necroinflammation initiated by donor organ cell death is implicated as a critical mediator of primary graft dysfunction, acute rejection, and chronic rejection. Ferroptosis is a form of regulated cell death that triggers post-transplantation inflammation and drives the activation of both innate and adaptive immune cells. There is a growing acceptance of the clinical relevance of ferroptosis to solid organ transplantation. Modulating ferroptosis may be a potentially promising strategy to reduce complications after organ transplantation.
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Base de datos:
MEDLINE
Asunto principal:
Trasplante de Órganos
/
Ferroptosis
Idioma:
En
Revista:
Cell Immunol
Año:
2023
Tipo del documento:
Article