ReviewAnnals of medicine2025
Bradykinin-bradykinin 2 receptor and oxidative stress.
Review in Annals of medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBradykinin (BK) and its primary receptor, the bradykinin 2 receptor (B2R), play pivotal roles in regulating oxidative stress. While B2R activation has traditionally been linked to elevated reactive oxygen species (ROS) and pro-apoptotic signalling, growing evidence indicates that, under specific contexts, it also exerts antioxidative and cytoprotective effects, enhancing cell survival, promoting proliferation and attenuating apoptosis.
methodsWe retrieved data from electronic databases PubMed, Web of Science, and ScienceDirect to systematically evaluate the bidirectional redox regulation mediated by B2R and propose a dynamic model that reconcile this apparent paradox.
resultsOur analysis underscores a tight association between the oxidative outcome of BK-B2R signalling and the duration of stimulation: multiple independent studies, together with our time-stratified analyses, suggest that prolonged BK exposure is more likely to elicit antioxidative responses. Mechanistically, an early, transient rise in ROS may activate cascades such as mitogen-activated protein kinase (MAPK), subsequently inducing adaptive antioxidant defences (e.g. catalase upregulation), thereby reframing 'controlled' ROS not as a purely toxic byproduct but as a signalling cue that sustains redox homeostasis.
conclusionIn sum, B2R is not a unidirectional pro-oxidant or antioxidant factor; rather, it functions as a context- and time-dependent modulator of oxidative stress. This refined understanding provides a conceptual framework for stage- or condition-specific B2R-targeted interventions in cardiovascular, neurological and inflammation-related disorders.
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