Heme Oxygenase-1 Modulation in Inflammatory Responses
Summary
Heme oxygenase-1 (HO-1) is a stress-inducible enzyme that catalyses the oxidative cleavage of free heme into biliverdin, carbon monoxide and ferrous iron. Beyond its canonical role in heme catabolism, HO-1 exerts potent antioxidant and anti-inflammatory effects through its reaction products and by modulating redox-sensitive signalling pathways. Induction of HO-1 in immune and parenchymal cells dampens pro-inflammatory cytokine production, promotes macrophage polarisation towards an anti-inflammatory phenotype and attenuates leukocyte adhesion in injured tissues. Conversely, dysregulated HO-1 activity can perturb iron homeostasis and, under certain conditions, contribute to ferroptotic cell death. The balance between cytoprotective and potentially deleterious outcomes underscores the therapeutic promise of targeted HO-1 modulation in sepsis, atherosclerosis, metabolic disorders and acute organ injury. Key regulatory inputs include the transcription factor Nrf2, hypoxia-inducible factor-1 and inflammatory stimuli, which collectively shape HO-1 expression and downstream inflammatory responses.
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Heme Oxygenase-1 Modulation in Inflammatory Responses publication trend
The graph below shows the total number of articles in heme oxygenase-1 modulation in inflammatory responses across all publications each year (not limited to Nature Index journals).
Technical terms
Heme oxygenase-1 (HO-1): An inducible enzyme that degrades free heme into biliverdin, carbon monoxide and iron, with antioxidant and anti-inflammatory roles.
Macrophage polarisation: The process by which macrophages adopt distinct functional phenotypes (pro-inflammatory M1 or anti-inflammatory M2) in response to environmental cues.
Nrf2 (NF-E2-related factor 2): A redox-sensitive transcription factor that upregulates HO-1 and other cytoprotective genes under oxidative stress.
Pyroptosis: A form of regulated cell death characterised by inflammasome activation, gasdermin-mediated membrane pores and release of pro-inflammatory cytokines.
Ferroptosis: An iron-dependent form of non-apoptotic cell death driven by lipid peroxide accumulation and oxidative stress.
References
- Effective protective mechanisms of HO-1 in diabetic complications: a narrative review. Cell Death Discovery (2024).
- Heme Oxygenase-1: An Anti-Inflammatory Effector in Cardiovascular, Lung, and Related Metabolic Disorders. Antioxidants (2022).
- Heme Oxgenase-1, a Cardinal Modulator of Regulated Cell Death and Inflammation. Cells (2021).
- Nuclear Heme Oxygenase-1 (HO-1) Modulates Subcellular Distribution and Activation of Nrf2, Impacting Metabolic and Anti-oxidant Defenses*. Journal of Biological Chemistry (2014).
- Hypoxia-inducible Factor-1 Mediates Transcriptional Activation of the Heme Oxygenase-1 Gene in Response to Hypoxia*. Journal of Biological Chemistry (1997).
- Heme Oxygenase-1 Signaling and Redox Homeostasis in Physiopathological Conditions. Biomolecules (2021).
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