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Figure 5. Potential HCM and aging-associated molecular events mediate the late onset of HCM among MYBPC3 gene carriers. (A) Differential expression and enrichment of trans-acting factors in MYBPC3 cis-elements regulate MYBPC3 transcription upon aging. (B) Age-associated altered splicing mechanisms result in aberrant splice products, and (C) dysregulated mRNA degradation through nonsense-mediated pathways determines the abundance of MYBPC3 mRNA available for translation. (D) Aging-induced differences in the expression of miRNAs might modulate MYBPC3 translation through post-transcriptional gene silencing. (E) Age-dependent changes in phosphorylation, (F) ubiquitination proteasome system, (G) and chaperone-mediated autophagy determine the sufficiency of MYBPC3 protein in preserving cardiac function (Figure Created with BioRender.com).