ArticleJournal of advanced research2026
EVA1A responds to endoplasmic reticulum stress to regulate renal fibrosis by promoting TGF-β signaling pathway.
Article in Journal of advanced research, 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
introductionRenal fibrosis is a common pathological hallmark of chronic kidney disease (CKD), and ultimately leads to end-stage renal disease. ER-stress and TGF-β signaling pathway activation play critical roles in renal fibrosis, but the precise mechanisms underlying the intricate interplay between ER-stress and TGF-β signaling pathway remain ambiguous. Our previous study has demonstrated that EVA1A responds to ER-stress to regulate hematopoietic stem cell regeneration; However, the function of EVA1A in renal fibrosis remains unexplored.
objectivesTo elucidate the role of EVA1A in TGF-β signaling regulation and renal fibrosis.
methodsWe characterized EVA1A expression changes in chronic kidney disease through single-cell RNA-seq data analysis, immunohistochemical staining and Western blot analysis. Eva1a conditional knockout mouse subjected to unilateral-ischemia-reperfusion-injury (UIRI) and unilateral-ureteral-obstruction (UUO), two well-established and widely used fibrosis-related CKD mouse models, were used to investigate the role of EVA1A in renal fibrosis. Subsequently, we characterized the interaction of EVA1A and TGF-β receptor type Ⅱ (TGFBR2) by co-immunoprecipitation and bimolecular-fluorescence-complementation (BiFC) assays to clarify the regulatory mechanism of EVA1A in TGF-β signaling.
resultsWe found that EVA1A was significantly upregulated in fibrotic kidneys from CKD patients and mice with UUO or UIRI treatment. Deletion of Eva1a significantly attenuated kidney fibrosis and damage in mice with UUO or UIRI treatment. Overexpression of EVA1A enhanced fibrosis levels in mice with UUO treatment and upregulated the expression of fibrosis-related proteins in cultured renal epithelial cells. Mechanistically, we found that ER stress upregulates EVA1A expression via CHOP in CKD mouse model. Subsequently, EVA1A interacted with BIP to stabilize and facilitate the secretion of TGFBR2 from ER to plasma membrane, thereby promoting TGF-β signaling activation and renal fibrosis.
conclusionDuring the progression of CKD, EVA1A serves as a sensor for ER stress and regulates renal fibrosis by promoting TGF-β signaling pathway activity.
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