Identification and validation of hypoxia responsive signature pathways in human cardiomyocytes

During ischemia, cardiomyocytes are unable to oxidize energetic substrates, which causes a significant depletion in ATP reserves. Heart remodels in response to increased workload by generating additional muscle mass in hypoxic microenvironment leading to impaired basic cardiac functions and hypertrophy.

The exact molecular mechanism of cardiac injury induced by hypoxia is not completely understood. The present study design to investigate the effect of hypoxia (1% O2) for 24 h in human AC16 cells by analyzing alteration in expression of cardiac markers and signature pathways using immunocytochemistry and next generation sequencing respectively. The gene set enrichment analysis and cytoscape software was used for data analysis and visualization respectively.This analysis revealed multiple pathways associated with hypoxia which provide valuable insight into molecular mechanisms underlying human cardiomyocytes, presenting potential targets addressing cardiac illnesses induced by hypoxia.