Abstract Body: Introduction
Pulmonary artery banding (PAB) has emerged as a potential strategy for left ventricular (LV) functional recovery in pediatric dilated cardiomyopathy (DCM), yet the underlying mechanisms remain unclear. This study establishes a small animal model to investigate the hemodynamic and molecular adaptations induced by PAB.

Methods
Sprague-Dawley rats underwent left anterior descending (LAD) artery ligation, followed by PAB one-week post-injury (LAD+PAB, n=13). Control groups included sham (n=16), PAB-only (n=16), and LAD-only (n=15). Echocardiography was performed weekly, and histological and molecular analyses were conducted four weeks after surgery.

Results
Compared to LAD-only rats, LAD+PAB animals exhibited positive LV remodeling with reduced LV end-diastolic volume (0.49±0.02 vs. 0.66±0.03 mL, p<0.001), improvement of LV ejection fraction (0.48±0.01 vs. 0.36±0.01, p<0.001), and normalization of mitral valve Doppler E/A (p<0.001). Histological analysis documented LV hypertrophy (p=0.005), increased LV cardiomyocyte diameter (p=0.001), and augmented neoangiogenesis (p=0.005) in LAD+PAB versus LAD-only hearts. Mechanistically, we observed reduced LV fibrosis (p=0.003) and fibroblast cellular senescence (p=0.02), and preserved phospholamban (PLN) phosphorylation in the LV of LAD+PAB versus LAD-only rats (pPLN/PLN, p=0.008).

Discussion
PAB induced a biventricular compensated hypertrophic response, which contributed to LV functional recovery after injury by recruiting residual myocardial reserve, limiting fibrosis, and maintaining calcium handling pathways. This adaptive response suggests that controlled RV pressure overload can trigger beneficial ventricular-ventricular interactions, promoting myocardial remodeling. The reduction in LV fibrosis and cellular senescence observed in PAB-treated animals supports the role of PAB in mitigating progressive myocardial injury. Increased neoangiogenesis in both ventricles suggests that PAB-induced hypertrophy is accompanied by vascular adaptation, which may enhance metabolic efficiency. Preservation of PLN phosphorylation may constitute another potential mechanism by which PAB sustains LV contractility through improved calcium cycling. This study provides mechanistic insights into PAB as a therapeutic strategy for LV dysfunction and as a potential bridge-to-recovery therapy in acute pediatric heart failure.