文献类型：期刊文献

英文题名：Bradykinin-bradykinin 2 receptor and oxidative stress

作者：Zhao, Jun[1];Wang, Zhuanping[2];Wang, Xuetao[1];Yang, Fangjun[1];Xi, Huirong[1];Wen, Jiantao[1];Zhang, Wenjing[1];Qiu, Xiaoming[1]

第一作者：赵娟

通信作者：Qiu, XM[1]

机构：[1]Gansu Univ Chinese Med, Gansu Prov Hosp TCM, Affiliated Hosp 1, Lanzhou, Peoples R China;[2]Lanzhou Univ, Hosp 2, Dept Endocrinol, Lanzhou, Peoples R China

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Gansu Prov Hosp TCM, Lanzhou 730000, Peoples R China.

年份：2025

卷号：57

期号：1

外文期刊名：ANNALS OF MEDICINE

收录：;Scopus(收录号：2-s2.0-105020733393);WOS:【SCI-EXPANDED(收录号:WOS:001606837400001)】；

基金：This study was supported by Major Joint Research Project of the Natural Science Foundation of Gansu Province, China (23JRRA1529, 24JRRA898), Longyuan Youth Innovation and Entrepreneurship Talent Team Project (2024QNTD07) and the Natural Science Foundation of Gansu Province (20JR10RA411).

语种：英文

外文关键词：KKS; bradykinin; oxidative stress

摘要：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.