Cardiomyocyte microRNAs (miRNA)

Cardiomyocyte microRNAs (miRNAs) regulating the cell cycle and survival represent a specialized class of small non-coding RNAs that orchestrate the gene expression programs necessary for heart muscle maintenance and repair. In the adult heart, cardiomyocytes possess extremely limited regenerative capacity, and these miRNAs serve as critical molecular switches that can either maintain the quiescent state or re-trigger the cell cycle to replace lost tissue (Eulalio et al., 2012, Nature). Key miRNAs such as miR-199a-3p and miR-590-3p have demonstrated the ability to induce robust cardiomyocyte proliferation by inhibiting negative regulators of the cell cycle, while others like miR-21 and miR-133 focus on enhancing cell survival and preventing apoptosis under ischemic conditions (Thum, 2014, Nature Reviews Cardiology). From a therapeutic perspective, these molecules are targeted using miRNA mimics to boost regenerative signaling or antagomirs to block miRNAs that contribute to pathological remodeling and heart failure (Täubel et al., 2021, Eur Heart J). Clinical development in this space, such as the miR-132 inhibitor CDR132L, highlights the potential for miRNA-based therapies to improve cardiac function in patients with heart failure (Sluijter et al., 2014, Circ Res). However, significant challenges remain, particularly regarding the precise delivery of these RNAs to cardiomyocytes and the mitigation of potential oncogenic risks associated with systemic cell cycle activation.

Other names

Cardiac microRNAsMyocyte miRNAsHeart-specific microRNAsRegenerative miRNAs

Post-transcriptional gene silencing via mRNA degradation or translational repression of target genes involved in cell cycle inhibition and pro-apoptotic signaling.