ArticleFrontiers in pharmacology2015
Kinin B1 receptor antagonism is equally efficient as angiotensin receptor 1 antagonism in reducing renal fibrosis in experimental obstructive nephropathy, but is not additive.
Article in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- The immunomodulatory potential of bradykinin signaling in autoimmune conditions.Frontiers in immunology · 2026Review
- Targeting Kinin B1R Attenuates Hypertension Through AT1R-Dependent Mechanisms.Circulation research · 2025Article
- Targeting CD13/Aminopeptidase N as a Novel Therapeutic Approach for Scleroderma Fibrosis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- Kinins: Locally formed peptides during inflammation with potential use in tissue regeneration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Kinin B1 Receptor Mediates Renal Injury and Remodeling in Hypertension.Frontiers in medicine · 2021Article
- Differential Expression of Kinin Receptors in Human Wet and Dry Age-Related Macular Degeneration Retinae.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Bradykinin 1 receptor blockade subdues systemic autoimmunity, renal inflammation, and blood pressure in murine lupus nephritis.Arthritis research & therapy · 2019Article
- Blockade of Bradykinin receptors worsens the dystrophic phenotype of mdx mice: differential effects for B1 and B2 receptors.Journal of cell communication and signaling · 2018Article
- Kidney tubules: intertubular, vascular, and glomerular cross-talk.Current opinion in nephrology and hypertension · 2016Review
- Hypoxia: The Force that Drives Chronic Kidney Disease.Clinical medicine & research · 2016Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRenal tubulointerstitial fibrosis is the pathological hallmark of chronic kidney disease (CKD). Currently, inhibitors of the renin-angiotensin system (RAS) remain the sole therapy in human displaying antifibrotic properties. Further antifibrotic molecules are needed. We have recently reported that the delayed blockade of the bradykinin B1 receptor (B1R) reduced the development of fibrosis in two animal models of renal fibrosis. The usefulness of new drugs also resides in outperforming the gold standards and eventually being additive or complementary to existing therapies.
methodsIn this study we compared the efficacy of a B1R antagonist (B1Ra) with that of an angiotensin type 1 receptor antagonist (AT1a) in the unilateral ureteral obstruction (UUO) model of renal fibrosis and determined whether bi-therapy presented higher efficacy than any of the drugs alone.
resultsB1R antagonism was as efficient as the gold-standard AT1a treatment. However, bitherapy did not improve the antifibrotic effects at the protein level. We sought for the reason of the absence of this additive effect by studying the expression of a panel of genes involved in the fibrotic process. Interestingly, at the molecular level the different drugs targeted different players of fibrosis that, however, in this severe model did not result in improved reduction of fibrosis at the protein level.
conclusionsAs the B1R is induced specifically in the diseased organ and thus potentially displays low side effects it might be an interesting alternative in cases of poor tolerability to RAS inhibitors.
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