ArticleNature communications2024
Multiple roles for hypoxia inducible factor 1-alpha in airway epithelial cells during mucormycosis.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- Molecular Mechanisms of Mucormycosis Pathogenesis: Host-Pathogen Interactions and Immune Evasion.Pathogens (Basel, Switzerland) · 2026Review
- Transcriptomic and proteomic profiling of pulmonary mucormycosis reveals a failed activation of host immune response.Frontiers in immunology · 2026Article
- circRNA-associated-ceRNA networks in patients with traumatic tracheal stenosis.Scientific reports · 2025Article
- Recognizing the Early Risk-Based Clinical Manifestations of Mucormycosis: Cornerstones for Improved Survival and Therapeutic Outcomes.Journal of fungi (Basel, Switzerland) · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
During pulmonary mucormycosis, inhaled sporangiospores adhere to, germinate, and invade airway epithelial cells to establish infection. We provide evidence that HIF1α plays dual roles in airway epithelial cells during Mucorales infection. We observed an increase in HIF1α protein accumulation and increased expression of many known HIF1α-responsive genes during in vitro infection, indicating that HIF1α signaling is activated by Mucorales infection. Inhibition of HIF1α signaling led to a substantial decrease in the ability of R. delemar to invade cultured airway epithelial cells. Transcriptome analysis revealed that R. delemar infection induces the expression of many pro-inflammatory genes whose expression was significantly reduced by HIF1α inhibition. Importantly, pharmacological inhibition of HIF1α increased survival in a mouse model of pulmonary mucormycosis without reducing fungal burden. These results suggest that HIF1α plays two opposing roles during mucormycosis: one that facilitates the ability of Mucorales to invade the host cells and one that facilitates the ability of the host to mount an innate immune response.
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Registered trials
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