ReviewFrontiers in immunology2025
HACE1 as a bridge between oxidative stress and autophagy.
Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Sigma-1 receptor protects against renal ischemia-reperfusion injury by enhancing mitophagy via Rac1 regulation.Renal failure · 2026Article
- Deltex 2 Mediates Oxidative Stress and Neurotoxicity in Freezing of Gait of Parkinson's Disease via the Notch2-Nrf2 Axis.CNS neuroscience & therapeutics · 2026Article
- HACE1 alleviates intervertebral disc degeneration by inhibiting ferroptosis in nucleus pulposus cells.Scientific reports · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HECT domain and ankyrin repeat-containing E3 ubiquitin-protein ligase 1 (HACE1) is a well-known tumor suppressor and is essential for embryonic development. In recent years, researchers have increasingly discovered that HACE1 plays a vital role in the pathological process of many degenerative diseases. HACE1 is regarded as a stress-responsive gene whose expression is induced by a variety of stress stimuli. The expression of HACE1 counters cell stress damage by promoting the expression of antioxidant genes and inhibiting ROS production from Rac1-dependent NADPH oxidase. Meanwhile, HACE1 serves as a crucial E3 ubiquitin ligase that activates autophagy by ubiquitinating autophagy-related receptors to clear irreversibly oxidized biomolecules within the cell. Therefore, HACE1 is essential for cellular survival by maintaining antioxidant defense mechanisms and autophagic flux. Pharmacological and genetic modulation of HACE1 expression holds potential therapeutic value in age-related diseases such as neurodegenerative disorders, cardiovascular diseases, and cancer.
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Registered trials
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