Accumulation of mitochondrial DNA mutations disrupts cardiac progenitor cell function and reduces survival

Abstract

Background: Mitochondrial DNA (mtDNA) mutations accumulate with age, but how this impacts cardiac progenitor cell (CPC) function is unknown. Results: MtDNA mutations disrupt mitochondrial function and reduce differentiation potential of CPCs. Conclusion: Preserving mtDNA integrity is critical for CPC homeostasis and regenerative potential. Significance: Increased understanding of pathways regulating progenitor cell function is critical for development of effective cell therapies.