Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/19038
Título
Oxidative Post-translational Protein Modifications upon Ischemia/Reperfusion Injury.
Autor(es)
Binek, Aleksandra CNIC | Castans, Celia CNIC | Jorge, Inmaculada CNIC | Bagwan, Navratan CNIC | Rodriguez, Jose Manuel CNIC | Fernandez-Jimenez, Rodrigo CNIC | Galan-Arriola, Carlos CNIC | Oliver, Eduardo CNIC | Gomez, Monica CNIC | Clemente-Moragón, Agustín | Ibáñez, Borja CNIC | Camafeita, Emilio CNIC | Vazquez, Jesus CNIC
Fecha de publicación
2024-01-16
Cita
Antioxidants (Basel). 2024 Jan 16;13(1):106.
Idioma
Inglés
Tipo de documento
journal article
Resumen
While reperfusion, or restoration of coronary blood flow in acute myocardial infarction, is a requisite for myocardial salvage, it can paradoxically induce a specific damage known as ischemia/reperfusion (I/R) injury. Our understanding of the precise pathophysiological molecular alterations leading to I/R remains limited. In this study, we conducted a comprehensive and unbiased time-course analysis of post-translational modifications (PTMs) in the post-reperfused myocardium of two different animal models (pig and mouse) and evaluated the effect of two different cardioprotective therapies (ischemic preconditioning and neutrophil depletion). In pigs, a first wave of irreversible oxidative damage was observed at the earliest reperfusion time (20 min), impacting proteins essential for cardiac contraction. A second wave, characterized by irreversible oxidation on different residues and reversible Cys oxidation, occurred at late stages (6-12 h), affecting mitochondrial, sarcomere, and inflammation-related proteins. Ischemic preconditioning mitigated the I/R damage caused by the late oxidative wave. In the mouse model, the two-phase pattern of oxidative damage was replicated, and neutrophil depletion mitigated the late wave of I/R-related damage by preventing both Cys reversible oxidation and irreversible oxidation. Altogether, these data identify protein PTMs occurring late after reperfusion as an actionable therapeutic target to reduce the impact of I/R injury.
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