ArticleMolecular medicine reports2021
HIGD‑1B inhibits hypoxia‑induced mitochondrial fragmentation by regulating OPA1 cleavage in cardiomyocytes.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
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- WTAP-mediated mRedox report : communications in free radical research · 2024Article
- HIGD1B, as a novel prognostic biomarker, is involved in regulating the tumor microenvironment and immune cell infiltration; its overexpression leads to poor prognosis in gastric cancer patients.Frontiers in immunology · 2024Article
- Genome-wide analysis of soybean hypoxia inducible gene domain containing genes: a functional investigation of GmHIGD3.Frontiers in plant science · 2024Article
- Mitochondrial Dynamics, Mitophagy, and Mitochondria-Endoplasmic Reticulum Contact Sites Crosstalk Under Hypoxia.Frontiers in cell and developmental biology · 2022Review
- Single Cell Transcriptomic Analysis Reveals Organ Specific Pericyte Markers and Identities.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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