ArticlePloS one2013
Bradykinin inhibits oxidative stress-induced cardiomyocytes senescence via regulating redox state.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Bradykinin-bradykinin 2 receptor and oxidative stress.Annals of medicine · 2025Review
- Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.European journal of medical research · 2025Review
- Snake Venom Components as Therapeutic Drugs in Ischemic Heart Disease.Biomolecules · 2023Review
- Effect of Kinins on the Hepatic Oxidative Stress in Mice Treated with a Methionine-Choline Deficient Diet.Biomedicines · 2023Article
- Metabolic Changes in Cardiac Aging.Reviews in cardiovascular medicine · 2023Review
- Bradykinin postconditioning protects rat hippocampal neurons after restoration of spontaneous circulation following cardiac arrest via activation of the AMPK/mTOR signaling pathway.Neural regeneration research · 2022Article
- Inorganic Nitrogen-Containing Aerosol Deposition Caused "Excessive Photosynthesis" of Herbs, Resulting in Increased Nitrogen Demand.Plants (Basel, Switzerland) · 2022Article
- HMolecular and cellular biochemistry · 2022Article
- The role of cellular senescence in cardiac disease: basic biology and clinical relevance.Nature reviews. Cardiology · 2022Review
- Insulin sensitivity in the aged heart is improved by down-regulation of KAT7Cell cycle (Georgetown, Tex.) · 2022Article
- Dynamic Mitochondrial Proteome Under Polyamines Treatment in Cardiac Aging.Frontiers in cell and developmental biology · 2022Article
- Bradykinin-Potentiating Activity of a Gamma-Irradiated Bioactive Fraction Isolated from Scorpion (Leiurus quinquestriatus) Venom in Rats with Doxorubicin-Induced Acute Cardiotoxicity: Favorable Modulation of Oxidative Stress and Inflammatory, Fibrogenic and Apoptotic Pathways.Cardiovascular toxicology · 2021Article
- Deficiency of telomere-associated repressor activator protein 1 precipitates cardiac aging in miceTheranostics · 2021Article
- Article
- Bradykinin and noradrenaline preconditioning influences level of antioxidant enzymes SOD, CuZn-SOD, Mn-SOD and catalase in the white matter of spinal cord in rabbits after ischemia/reperfusion.European journal of histochemistry : EJH · 2019Article
- Article
- Antioxidant and Antisenescence Effects of Bergamot Juice.Oxidative medicine and cellular longevity · 2018Article
- EETs reduces LPS-induced hyperpermeability by targeting GRP78 mediated Src activation and subsequent Rho/ROCK signaling pathway.Oncotarget · 2017Article
- The destiny of the resistance/susceptibility against GCRV is controlled by epigenetic mechanisms in CIK cells.Scientific reports · 2017Article
- The Citrus Flavanone Naringenin Protects Myocardial Cells against Age-Associated Damage.Oxidative medicine and cellular longevity · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCell senescence is central to a large body of age related pathology, and accordingly, cardiomyocytes senescence is involved in many age related cardiovascular diseases. In consideration of that, delaying cardiomyocytes senescence is of great importance to control clinical cardiovascular diseases. Previous study indicated that bradykinin (BK) protected endothelial cells from senescence induced by oxidative stress. However, the effects of bradykinin on cardiomyocytes senescence remain to be elucidated. In this study, we investigated the effect of bradykinin on H2O2-induced H9C2 cells senescence. METHODS AND
resultsBradykinin pretreatment decreased the senescence induced by H2O2 in cultured H9C2 cells in a dose dependent manner. Interestingly, 1 nmol/L of BK almost completely inhibited the increase in senescent cell number and p21 expression induced by H2O2. Since H2O2 induces senescence through superoxide-induced DNA damage, we also observed the DNA damage by comet assay, and BK markedly reduced DNA damage induced by H2O2, and moreover, BK treatment significantly prevented reactive oxygen species (ROS) production in H9C2 cells treated with H2O2. Importantly, when co-incubated with bradykinin B2 receptor antagonist HOE-140 or eNOS inhibitor N-methyl-L-arginine acetate salt (L-NAME), the protective effects of bradykinin on H9C2 senescence were totally blocked. Furthermore, BK administration significantly prevented the increase in nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity characterized by increased ROS generation and gp91 expression and increased translocation of p47 and p67 to the membrane and the decrease in superoxide dismutase (SOD) activity and expression induced by H2O2 in H9C2 cells, which was dependent on BK B2 receptor mediated nitric oxide (NO) release.
conclusionsBradykinin, acting through BK B2 receptor induced NO release, upregulated antioxidant Cu/Zn-SOD and Mn-SOD activity and expression while downregulating NADPH oxidase activity and subsequently inhibited ROS production, and finally protected against cardiomyocytes senescence induced by oxidative stress.
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