ArticleClinical and experimental pharmacology & physiology2026
Mechanisms of IL-17A Neutralisation in Alleviating Renal Fibrosis and Inflammation in Spontaneously Hypertensive Rats.
Article in Clinical and experimental pharmacology & physiology, 2026. 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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Abstract
objectiveThis study investigated the therapeutic effects and mechanisms of IL-17A neutralisation on renal interstitial fibrosis and inflammation in spontaneously hypertensive rats (SHRs).
methodsSHRs were treated with an IL-17A-neutralising antibody (NAb) for 20 weeks. Blood pressure and renal function were monitored. Renal tissues were analysed for histopathology, macrophage polarisation, epithelial-mesenchymal transition (EMT), inflammatory cytokines, and relevant signalling pathways.
resultsIL-17A NAb treatment significantly attenuated hypertension progression and improved renal function. It also ameliorated renal fibrosis and histopathological damage. Mechanistically, IL-17A neutralisation suppressed M2 macrophage polarisation and downregulated the TGF-β/Smad pathway, an effect associated with attenuated extracellular matrix (ECM) remodelling. This was accompanied by reduced levels of pro-inflammatory cytokines and inhibition of key inflammatory signalling pathways, including JAK/STAT, PI3K/AKT, and NF-κB.
conclusionOur findings demonstrate that IL-17A neutralisation alleviates renal fibrosis and inflammation in SHRs. The protective effects are associated with the inhibition of M2 macrophage polarisation, suppression of the TGF-β/Smad pathway and the associated EMT process, and attenuation of systemic and renal inflammation, concomitant with the coordinated downregulation of the JAK/STAT, PI3K/AKT, and NF-κB signalling pathways.
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