{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T04:00:44Z","timestamp":1773028844446,"version":"3.50.1"},"reference-count":44,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T00:00:00Z","timestamp":1768867200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T00:00:00Z","timestamp":1768867200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Basic Clin Pharma Tox"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Chronic kidney disease (CKD) remains a significant global health burden despite recent advances in pharmacotherapy, including sodium\u2010glucose cotransporter 2 (SGLT2) inhibitors and mineralocorticoid receptor antagonists. Renal fibrosis, a central pathological hallmark of CKD progression, is mediated by persistent inflammation and macrophage activation, wherein the kallikrein\u2013kinin system\u2014particularly kinin receptors\u2014plays a critical role. Emerging evidence supports the therapeutic potential of dual kinin receptor antagonism, especially targeting B1R, though the precise molecular mechanisms remain incompletely understood, necessitating further investigation. To elucidate the role of kinin receptors in renal injury, male C57BL\/6 mice were subjected to folic acid\u2010induced nephropathy and treated with either the B1R antagonist R715 or the B2R antagonist HOE140. Treatments were administered pre\u2010 and postfolic acid injection. Renal function was evaluated via serum creatinine, blood urea nitrogen and urine analyses. Renal tissues underwent histopathological assessment and gene expression profiling to assess injury and fibrotic responses. B2R antagonism (HOE140) failed to attenuate acute tubular injury but ameliorated chronic damage by downregulating proinflammatory mediators and upregulating anti\u2010inflammatory markers. In contrast, B1R blockade (R715) exacerbated acute kidney injury yet mitigated chronic fibrosis, improving renal function and reducing profibrotic gene expression. These findings delineate distinct, time\u2010dependent roles of B1R and B2R in modulating macrophage polarization (M1\/M2) and fibrogenesis, identifying potential targets for antifibrotic therapies.<\/jats:p>","DOI":"10.1111\/bcpt.70189","type":"journal-article","created":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T10:13:26Z","timestamp":1768904006000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Antagonism of Kinin Receptors B1 and B2 Attenuates Folic Acid\u2010Induced Tubulointerstitial Fibrosis in Mice"],"prefix":"10.1111","volume":"138","author":[{"given":"Gabriel\u00a0Rufino","family":"Estrela","sequence":"first","affiliation":[{"name":"Department of Biophysics Federal University of S\u00e3o Paulo  S\u00e3o Paulo Brazil"},{"name":"Discipline of Nephrology Federal University of S\u00e3o Paulo  S\u00e3o Paulo 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