Ribosomal Remodeling and Translational Suppression in the Post-Arrest Heart

Cardiac arrest suppresses myocardial protein synthesis in mice, with ribosome activity remaining suppressed for at least 24 h after resuscitation.

• Why it matters: No pharmacologic therapies improve post-arrest outcomes, and the molecular basis of acute myocardial dysfunction after CA is incompletely understood.
• What they did: Using complementary porcine and murine CA models, the study profiled left ventricular tissue with RNA sequencing in pigs and multi-omic profiling (RNA sequencing, ribosome profiling, proteomics) across time points in mice.
• The result: In pigs, translation-related and cytosolic ribosomal protein transcripts increased with ischemic burden, while in mice ribosome- and translation-related pathways were consistently altered and 24 h showed disruptions in ion homeostasis and conduction-linked pathways linked to translational suppression.

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