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The study provides compelling evidence linking RyR2-mediated Ca²⁺ leak to cognitive dysfunction in heart failure. However, some clarifications would strengthen the interpretation of the findings. Could the authors elaborate on whether RyR2 post-translational modifications are a direct consequence of heart failure or if they may be predisposing factors?
The study presents strong evidence linking RyR2-mediated Ca²⁺ leak to cognitive dysfunction in heart failure. Regarding RyR2 post-translational modifications (PTMs), existing data indicate that hyperphosphorylation, oxidation, and nitrosylation of RyR2 are commonly observed in heart failure models. While these modifications are widely considered a consequence of pathological remodeling, some studies suggest that pre-existing RyR2 dysfunction could predispose individuals to cardiac and neurological impairments. However, distinguishing causality remains challenging due to the interplay of systemic oxidative stress, metabolic dysregulation, and neuroinflammation in heart failure. Further longitudinal and mechanistic studies are needed to determine whether RyR2 PTMs act as early biomarkers or secondary adaptations in disease progression.