ArticleMolecular medicine reports2019
Effects of nuclear respiratory factor‑1 on apoptosis and mitochondrial dysfunction induced by cobalt chloride in H9C2 cells.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Pharmacological approaches to enhance mitochondrial biogenesis: focus on PGC-1Α, AMPK, and SIRT1 in cellular health.Molecular biology reports · 2025Pooled it
- A Brief Description of the Cellular Mechanisms Involved in Cardiac Chemical Hypoxia.Cardiovascular toxicology · 2026Review
- Nuclear respiratory factor-1 promotes CFLAR transcription in H9C2 cardiomyocytes, protecting them against hypoxia-induced apoptosis.Molecular biology reports · 2025Article
- Hong-Bai-Lan-Shen Extract Alleviates the CoClVeterinary sciences · 2025Article
- Rhabdastrellosides A and B: Two New Isomalabaricane Glycosides from the Marine SpongeMarine drugs · 2023Article
- Nuclear respiratory factor 1 promotes the progression of EBV-associated gastric cancer and maintains EBV latent infection.Virus genes · 2023Article
- TRPA1 as Target in Myocardial Infarction.International journal of molecular sciences · 2023Article
- Promoting cardioprotection with fenugreek: Insights from CoClIranian journal of basic medical sciences · 2023Article
- Studies on Regulation of Global Protein Profile and Cellular Bioenergetics of Differentiating SH-SY5Y Cells.Molecular neurobiology · 2022Article
- Nesfatin-1 protects H9c2 cardiomyocytes against cobalt chloride-induced hypoxic injury by modulating the MAPK and Notch1 signaling pathways.Journal of biological research (Thessalonike, Greece) · 2021Article
- Integrated On-Chip 3D Vascular Network Culture under Hypoxia.Micromachines · 2020Article
- Identification of microRNA‑363‑3p as an essential regulator of chondrocyte apoptosis in osteoarthritis by targeting NRF1 through the p53‑signaling pathway.Molecular medicine reports · 2020Article
- Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia‑induced apoptosis occurs in various diseases. Cobalt chloride (CoCl2) is a hypoxia mimic agent that is frequently used in studies investigating the mechanisms of hypoxia. Nuclear respiratory factor‑1 (NRF‑1) is a transcription factor with an important role in the expression of mitochondrial respiratory and mitochondria‑associated genes. However, few studies have evaluated the effects of NRF‑1 on apoptosis, particularly with regard to damage caused by CoCl2. In the present study, the role of NRF‑1 in mediating CoCl2‑induced apoptosis was investigated using cell viability analysis, flow cytometry, fluorescence imaging, western blotting analysis, energy metabolism analysis and reverse transcription‑quantitative polymerase chain reaction. The present results revealed that the apoptosis caused by CoCl2 could be alleviated by NRF‑1. Furthermore, overexpression of NRF‑1 increased the expression of B‑cell lymphoma‑2, hypoxia inducible factor‑1α and NRF‑2. Also, cell damage induced by CoCl2 may be associated with depolarization of mitochondrial membrane potential, and NRF‑1 suppressed this effect. Notably, the oxygen consumption rate (OCR) was reduced in CoCl2‑treated cells, whereas overexpression of NRF‑1 enhanced the OCR, suggesting that NRF‑1 had protective effects. In summary, the present study demonstrated that NRF‑1 protected against CoCl2‑induced apoptosis, potentially by strengthening mitochondrial function to resist CoCl2‑induced damage to H9C2 cells. The results of the present study provide a possible way for the investigation of myocardial diseases.
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