When an immunomodulatory, sustained release formulation of polymeric microparticles (MP) delivering CCL22 (CCL22MP), was administered after cardiotoxin (CTx)-mediated muscle injury, significantly improved limb function was observed on days 3 and 5 post injury...Analysis of the local immune populations revealed augmented Treg concentrations, as well as altered infiltrating myeloid populations towards pro-repair subsets. These findings reveal that amplifying local Treg to damaged areas improves outcomes, thus offering a translationally promising approach after muscle injury.
Common in vivo injury models include cardiotoxin (CTX), freeze-induced (FI) and eccentric contraction (EC) injuries...These findings reveal distinct regeneration trajectories across injury models that differ in both mode and severity, highlighting potential molecular and cellular mechanisms that warrant further investigation. Our validated model provides a computational framework for future systematic exploration of how injury severity and other initial conditions independently influence regeneration outcomes, which could inform tailored therapeutic strategies in preclinical studies.
Iron deficiency impairs skeletal muscle regeneration by stabilizing HIF-2α in MuSC, inducing Rb1 RNA expression, and repressing E2F-dependent proliferation. Transient HIF-2α inhibition rescues MuSC proliferation and muscle repair under iron-deficient conditions, highlighting HIF-2α as a potential therapeutic target to counteract sarcopenia in aging and chronic diseases.
7 months ago
Journal
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RB1 (RB Transcriptional Corepressor 1) • EPAS1 (Endothelial PAS domain protein 1)
Drug sensitivity analysis identified compounds such as sotrastaurin (-10.2 kcal/mol), austocystin D (-9.7 kcal/mol), and tivozanib (-9.3 kcal/mol) as potentially effective inhibitors based on predicted binding affinity. Our integrative analysis highlights HTR1F as a potential biomarker associated with prognosis, immune modulation, and drug sensitivity across multiple cancer types. These findings provide a foundation for future experimental and clinical studies to explore HTR1F-targeted therapies.