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Anti-Ferroptotic Treatment Deteriorates Myocardial Infarction by Inhibiting Angiogenesis and Altering Immune Response.
Stairley, Rebecca A; Trouten, Allison M; Li, Shuang; Roddy, Patrick L; DeLeon-Pennell, Kristine Y; Lee, Kyu-Ho; Sucov, Henry M; Liu, Chun; Tao, Ge.
Afiliación
  • Stairley RA; Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Trouten AM; Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Li S; Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Roddy PL; Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
  • DeLeon-Pennell KY; Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Lee KH; Division of Cardiology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Sucov HM; Research Service, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC 29401, USA.
  • Liu C; Department of Medicine Digestive Disease Research Core Center, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Tao G; Department of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
Antioxidants (Basel) ; 13(7)2024 Jun 26.
Article en En | MEDLINE | ID: mdl-39061839
ABSTRACT
Mammalian cardiomyocytes have limited regenerative ability. Cardiac disease, such as congenital heart disease and myocardial infarction, causes an initial loss of cardiomyocytes through regulated cell death (RCD). Understanding the mechanisms that govern RCD in the injured myocardium is crucial for developing therapeutics to promote heart regeneration. We previously reported that ferroptosis, a non-apoptotic and iron-dependent form of RCD, is the main contributor to cardiomyocyte death in the injured heart. To investigate the mechanisms underlying the preference for ferroptosis in cardiomyocytes, we examined the effects of anti-ferroptotic reagents in infarcted mouse hearts. The results revealed that the anti-ferroptotic reagent did not improve neonatal heart regeneration, and further compromised the cardiac function of juvenile hearts. On the other hand, ferroptotic cardiomyocytes played a supportive role during wound healing by releasing pro-angiogenic factors. The inhibition of ferroptosis in the regenerating mouse heart altered the immune and angiogenic responses. Our study provides insights into the preference for ferroptosis over other types of RCD in stressed cardiomyocytes, and guidance for designing anti-cell-death therapies for treating heart disease.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Antioxidants (Basel) Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Antioxidants (Basel) Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza