fig3

Figure 3. Schematic representation of MYBPC3 gene variant-associated molecular events and age-associated hallmarks triggering hypertrophic signals in cardiac muscles. The nonsense-mediated mRNA degradation, ubiquitin proteosome-mediated protein degradation, alternate splicing, protein phosphorylation, and deregulated calcium sensing are the most common events in the HCM phenotype with MYBPC3 mutations. The hallmarks of aging - namely, genomic instability, inflammation, autophagy, mitochondrial dysfunction, deregulated nutrient sensing, altered cellular senescence, protein homeostasis, and epigenetic alterations - activate aging-associated pathways in cardiac muscle cells. Both genetic mutation and aging-associated events generate pro-hypertrophic signals and induce hypertrophic phenotype affecting the cardiac muscle cell structure and function.