Key result
Endothelial Ino80 deletion induces ventricular non-compaction by altering angiocrine factors to inhibit cardiomyocyte proliferation.
Why the study?
The mechanisms and cell types involved in ventricular non-compaction cardiomyopathy, a common genetic cardiomyopathy, are poorly understood.
Endocardial and endothelial cells regulate myocardial compaction through secreted angiocrine factors, and their dysregulation contributes to ventricular non-compaction.
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Dysregulated endothelial angiocrines may drive non-compaction features in mice; leaves open their causal role and therapeutic targeting in human LVNC.
Rhee et al. (2020) studied Left ventricular non-compaction. Endothelial Ino80 deletion and angiocrine factor manipulation vs. Control mice/cells was evaluated on Cardiomyocyte proliferation and maturation. Endothelial Ino80 deletion induced ventricular non-compaction by downregulating the proliferation-promoting angiocrine Col15a1 and upregulating factors (Tgfbi, Igfbp3, Isg15, Adm) that inhibit cardiomyocyte proliferation and promote premature maturation.
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