ArticleRedox biology2014
Mitochondria-targeted heme oxygenase-1 induces oxidative stress and mitochondrial dysfunction in macrophages, kidney fibroblasts and in chronic alcohol hepatotoxicity.
Article in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 161 citations in OpenAlex.
- Blood-brain barrier-penetrant nanotherapy inhibits haem oxygenase-1-mediated ferroptosis for post-resuscitation neuroprotection.Nature communications · 2026Article
- Kaempferol Alleviates Aflatoxin B1-Induced Liver Injury by Mitigating Oxidative Stress.Nutrients · 2026Article
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- Comparative evaluation of PEGylated bovine hemoglobin as a perfusate in rat ex vivo lung perfusion.Respiratory research · 2026Article
- CD73Nature communications · 2026Article
- THC and CBD Induce Heme Oxygenase-1-Dependent Cell Death and Trigger Mitochondrial Dysfunction in Human Melanoma and Cutaneous Squamous Cell Carcinoma Cells.Antioxidants (Basel, Switzerland) · 2026Article
- A novel transdermal curcumin gel shows potential in improving cardiac bioenergetic functions in Berkeley sickle cell mice.Blood vessels, thrombosis & hemostasis · 2026Article
- Heme and CO metabolism by the canonical human heme oxygenases.Journal of inorganic biochemistry · 2026Review
- Article
- Induced pluripotent stem cell-derived mesenchymal stem cells (iMSCs) inhibit M1 macrophage polarization and reduce alveolar bone loss associated with periodontitis.Stem cell research & therapy · 2025Article
- ROMO1: A Distinct Mitochondrial Protein with Dual Roles in Dynamics and Function.Antioxidants (Basel, Switzerland) · 2025Article
- Carbon Monoxide Stimulates Chondrocyte Mitochondria and Protects Mitochondria During Cartilage Injury.Antioxidants (Basel, Switzerland) · 2025Article
- Understanding and using Animal Models of Hepatotoxicity.Current pharmaceutical design · 2025Review
- Sphingosine kinase 2 (SphK2) depletion alters redox metabolism and enhances inflammation in a diet-induced MASH mouse model.Hepatology communications · 2024Article
- Palmitoylcarnitine impairs immunity in decompensated cirrhosis.JHEP reports : innovation in hepatology · 2024Article
- Advances in the Effects of Heat Stress on Ovarian Granulosa Cells: Unveiling Novel Ferroptosis Pathways.Veterinary sciences · 2024Review
- A non-canonical role of ELN protects from cellular senescence by limiting iron-dependent regulation of gene expression.Redox biology · 2024Article
- Cyclophosphamide induces ovarian granulosa cell ferroptosis via a mechanism associated with HO-1 and ROS-mediated mitochondrial dysfunction.Journal of ovarian research · 2024Article
- Nanoparticles with intermediate hydrophobicity polarize macrophages to plaque-specific Mox phenotype via Nrf2 and HO-1 activation.Journal of hazardous materials · 2024Article
- Role of ferroptosis in the pathogenesis of heart disease.Frontiers in physiology · 2024Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The inducible form of Heme Oxygenase-1 (HO-1), a major endoplasmic reticulum (ER) associated heme protein, is known to play important roles in protection against oxidative and chemical stress by degrading free heme released from degradation of heme proteins. In this study we show that induced expression of HO-1 by subjecting macrophage RAW-264.7 cells to chemical or physiological hypoxia resulted in significant translocation of HO-1 protein to mitochondria. Transient transfection of COS-7 cells with cloned cDNA also resulted in mitochondrial translocation of HO-1. Deletion of N-terminal ER targeting domain increased mitochondrial translocation under the transient transfection conditions. Mitochondrial localization of both intact HO-1 and N-terminal truncated HO-1 caused loss of heme aa-3 and cytochrome c oxidase (CcO) activity in COS-7 cells. The truncated protein, which localizes to mitochondria at higher levels, induced substantially steeper loss of CcO activity and reduced heme aa3 content. Furthermore, cells expressing mitochondria targeted HO-1 also induced higher ROS production. Consistent with dysfunctional state of mitochondria induced by HO-1, the mitochondrial recruitment of autophagy markers LC-3 and Drp-1 was also increased in these cells. Chronic ethanol feeding in rats also caused an increase in mitochondrial HO-1 and decrease in CcO activity. These results show that as opposed to the protective effect of the ER associated HO-1, mitochondria targeted HO-1 under normoxic conditions induces mitochondrial dysfunction.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.