Summary
This review examines the molecular mechanisms by which chemopreventive phytochemicals and synthetic compounds activate the Keap1–Nrf2 signalling pathway, a key cellular defence system against oxidative stress and carcinogenesis. The authors detail how thiol-reactive compounds disrupt Keap1-mediated degradation of Nrf2, allowing nuclear accumulation and transactivation of antioxidant response element-driven genes encoding detoxification and protective enzymes. The review synthesises evidence on ARE structure, species differences in Nrf2-target gene batteries, and the critical cysteine residues in Keap1 required for this adaptive cellular response.
Regional applicability
This is a cellular and molecular mechanism review with no geographic constraints. The findings are applicable globally and to United Kingdom research and practice, as they describe fundamental biochemical pathways relevant to understanding how dietary phytochemicals (e.g. from cruciferous vegetables, polyphenols) may support cellular defence mechanisms. Applicability depends on translation to functional food and dietary intervention studies in human populations.
Key measures
Nrf2 protein accumulation, ARE-driven gene expression, ubiquitylation status, Keap1 cysteine residues, antioxidant enzyme and drug-metabolising enzyme induction
Outcomes reported
The review describes how chemopreventive agents (synthetic compounds and phytochemicals) activate the Nrf2 transcription factor pathway, leading to upregulation of antioxidant and detoxification genes. It examines the molecular mechanisms of Keap1-dependent regulation of Nrf2 and the antioxidant response elements (ARE) that control target gene expression.
Topic tags
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