ArticleCellular & molecular biology letters2026
Chlorogenic acid mitigates calcium oxalate monohydrate crystal-induced epithelial-to-mesenchymal transition in renal epithelial cells via suppression of HSP60 expression and p38 signaling.
Article in Cellular & molecular biology letters, 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
backgroundEpithelial-to-mesenchymal transition (EMT) is a prominent process involved in kidney fibrosis. Calcium oxalate monohydrate (COM), a crystalline composition predominantly found in renal stones, is one of the known stimuli that can trigger the EMT process. Chlorogenic acid (CGA), a phenolic hydroxycinnamate naturally found in several plants (especially coffee beans), has several health benefits, including antifibrotic properties. However, the mechanisms underlying its preventive effects against COM-induced EMT in renal epithelial cells remain unclear.
methodsHerein, Madin-Darby canine kidney (MDCK) renal epithelial cells were exposed to COM crystals without or with CGA pre-/cotreatment and were subjected to various assays, including morphological examination, measurement of cell spindle index, transepithelial resistance (TER) measurement, immunofluorescence staining of EMT markers, and western blotting of p38 signaling proteins. Additionally, label-free quantitative proteomics using nanoLC-ESI-LTQ-Orbitrap MS/MS and functional enrichment analyses were carried out, followed by functional validation of the essential role of heat shock protein 60 (HSP60) using a small interfering RNA (siRNA)-based knockdown method.
resultsAs expected, COM induced the EMT process as shown by increases in spindle index and mesenchymal marker (vimentin) but decreases in TER and epithelial marker (ZO-1). Mechanistically, these changes were accompanied with activation of p38 signaling. However, CGA pre-/cotreatment successfully prevented all these COM-induced changes. Label-free quantitative proteomics revealed significantly altered levels of 167 cellular proteins caused by COM. Among these, 55 proteins were completely preserved by CGA. Protein-protein interaction network illustrated HSP60 as a hub of these interacting proteins. While COM increased the HSP60 level, CGA successfully preserved this protein at its basal level. Moreover, knockdown of HSP60 expression by small interfering RNA could also prevent COM-induced EMT and p38 activation.
conclusionsThese data indicate that CGA mitigates COM-induced EMT via suppression of HSP60 expression and p38 signaling activated by COM crystals.
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