HIGD‑1B inhibits hypoxia‑induced mitochondrial fragmentation by regulating OPA1 cleavage in cardiomyocytes

The dynamic regulation of mitochondrial morphology is key for eukaryotic cells to manage physiological challenges. Therefore, it is important to understand the molecular basis of mitochondrial dynamic regulation. The aim of the present study was to explore the role of HIG1 hypoxia inducible domain family member 1B (HIGD‑1B) in hypoxia‑induced mitochondrial fragmentation. Protein expression was determined via western blotting. Immunofluorescence assays were performed to detect the subcellular location of HIGD‑1B. Cell Counting Kit‑8 assays and flow cytometry were carried out to measure cell viability and apoptosis, respectively. Protein interactions were evaluated by co‑immunoprecipitation. In the present study, it was found that HIGD‑1B serves a role in cell survival by maintaining the integrity of the mitochondria under hypoxic conditions. Knockdown of HIGD‑1B promoted mitochondrial fragmentation, while overexpression of HIGD‑1B increased survival by preventing activation of caspase‑3 and ‑9. HIGD‑1B expression was associated with cell viability and apoptosis in cardiomyocytes. Furthermore, HIGD‑1B delayed the cleavage process of optic atrophy 1 (OPA1) and stabilized mitochondrial morphology by interacting with OPA1. Collectively, the results from the present study identified a role for HIGD‑1B as an inhibitor of the mitochondrial fission in cardiomyocytes.