Therapeutic Effect of Myostatin/Activin Blockage and Dietary Restriction in Modulation of Platelet Activation Markers of Progeroid Mouse Model

Aging-related decline in hematopoietic and platelet function is a hallmark of DNA repair deficiency syndromes, yet the impact of metabolic and pharmacological interventions on platelet biology in this context remains unclear. This study addresses this gap by investigating whether dietary restriction (DR) and myostatin/activin blockade through soluble Activin Receptor Type IIB (sActRIIB) can modulate platelet activation markers—GPIbα and P-Selectin—in a progeroid mouse model (Ercc1Δ/-). While DNA repair-deficient mice exhibited significantly reduced GPIbα expression compared to wild-type controls, sActRIIB treatment showed a modest, though non-significant, improvement. In contrast, DR alone or combined with sActRIIB had negligible effects. P-Selectin levels remained unchanged between mutant and control mice; however, sActRIIB treatment significantly suppressed its expression, indicating a potential anti-inflammatory effect. These findings suggest that myostatin/activin pathway inhibition may offer a partial therapeutic benefit in modulating platelet activation in progeroid models, whereas dietary restriction appears insufficient. It is important to conduct further studies to investigate specific, combinatorial application in the restoration of platelet homeostasis in DNA repair-deficient aging diseases.