ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Zyxin protects against hypertensive nephropathy by restraining FAK/Skp2-CDK8/YAP signaling in tubular epithelial cells.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 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
backgroundTubulointerstitial fibrosis and inflammation are hallmark pathological features of hypertensive nephropathy (HN), yet the underlying molecular mechanisms remain elusive. Zyxin, a focal adhesion protein, has been implicated in hypertension-related pathologies, but its specific role in HN-induced tubulointerstitial injury remains undefined.
methodsAn HN murine model was established via a multi‑hit DOCA/Ang II + uninephrectomy + high salt approach. Intrarenal zyxin was overexpressed using adeno-associated virus. In vitro, HK-2 cells were stimulated with Ang II, and zyxin levels were modulated via lentiviral transduction. Renal function, inflammation, and fibrosis were evaluated through biochemical assays and molecular signaling analysis.
resultsZyxin was significantly downregulated in the renal tubules of HN mice and Ang II-treated HK-2 cells. Zyxin overexpression significantly improved renal function and attenuated tubulointerstitial injury, with a representative reduction of approximately 40% in the expression of fibrotic markers. These protective effects occurred independently of blood pressure changes. Mechanistically, zyxin reduction is linked to Ang II-induced calpain activation. The resulting zyxin depletion potentially disinhibits the FAK/Skp2 axis and enhances CDK8/YAP signaling, which may contribute to renal inflammation and interstitial fibrosis.
conclusionsThese findings support a model in which zyxin acts as a protective factor in the renal tubules during HN, suggesting its potential as a novel therapeutic target.
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