Key result
Cardiac progenitor cell secretome and ENO1 improve contractility and mitochondrial function in hypoxic cardiomyocytes.
Population
100 cardiac tissue samples from children undergoing open heart surgery, matured stem cell-derived…
Design
Preclinical
Authors
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Metabolic regulators, specifically enolase-1 (ENO1), derived from the pediatric heart secretome can improve contractile function and mitochondrial respiration in injured cardiomyocytes, suggesting a potential novel metabolic therapy for heart failure.
p-value: p=<0.01
Metabolic regulators, specifically enolase-1 (ENO1), derived from the pediatric heart secretome can improve contractile function and mitochondrial respiration in injured cardiomyocytes, suggesting a potential novel metabolic therapy for heart failure.
Langari et al. (2025) studied Heart failure / Ischemic cardiac injury (n=100). Pediatric cardiac progenitor cell secretome and Enolase-1 (ENO1) vs. Untreated / Hypoxia control was evaluated on Tissue contractility, mitochondrial mass and polarization, basal and maximal respiration, and ATP/ADP ratio (p=<0.01). Treatment with pediatric cardiac progenitor cell secretome and specifically Enolase-1 (ENO1) improved tissue contractility, mitochondrial function, and respiration in hypoxic cardiomyocytes (p<0.01).
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