ArticleInternational journal of molecular sciences2022
Endoglin Is an Important Mediator in the Final Common Pathway of Chronic Kidney Disease to End-Stage Renal Disease.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- The EAT-Lancet planetary health diet and risk of incident chronic kidney disease.CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne · 2026Article
- Urine-Derived CD105-Positive Exosome Promotes Macrophage M1 Polarization Through the TGF-β1/Smad3 Signaling Axis To Exacerbate Lupus Nephritis.Inflammation · 2025Article
- Tumor-Associated Macrophages in Lung Cancer: Origins, Functional Heterogeneity, and Therapeutic Implications.Journal of inflammation research · 2025Review
- Single-Cell Sequencing Uncovers a TMSB10-Expressing Fibroblast Subpopulation Driving Renal Fibrosis in Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Novel genomic variants influencing methotrexate delayed clearance in pediatric patients with acute lymphoblastic leukemia.Frontiers in pharmacology · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Chronic kidney disease (CKD) is a slow-developing, progressive deterioration of renal function. The final common pathway in the pathophysiology of CKD involves glomerular sclerosis, tubular atrophy and interstitial fibrosis. Transforming growth factor-beta (TGF-β) stimulates the differentiation of fibroblasts towards myofibroblasts and the production of extracellular matrix (ECM) molecules, and thereby interstitial fibrosis. It has been shown that endoglin (ENG, CD105), primarily expressed in endothelial cells and fibroblasts, can function as a co-receptor of TGF signaling. In several human organs, endoglin tends to be upregulated when chronic damage and fibrosis is present. We hypothesize that endoglin is upregulated in renal interstitial fibrosis and plays a role in the progression of CKD. We first measured renal endoglin expression in biopsy samples obtained from patients with different types of CKD, i.e., IgA nephropathy, focal segmental glomerulosclerosis (FSGS), diabetic nephropathy (DN) and patients with chronic allograft dysfunction (CAD). We showed that endoglin is upregulated in CAD patients (p < 0.001) and patients with DN (p < 0.05), compared to control kidneys. Furthermore, the amount of interstitial endoglin expression correlated with eGFR (p < 0.001) and the amount of interstitial fibrosis (p < 0.001), independent of the diagnosis of the biopsies. Finally, we investigated in vitro the effect of endoglin overexpression in TGF-β stimulated human kidney fibroblasts. Overexpression of endoglin resulted in an enhanced ACTA2, CCN2 and SERPINE1 mRNA response (p < 0.05). It also increased the mRNA and protein upregulation of the ECM components collagen type I (COL1A1) and fibronectin (FN1) (p < 0.05). Our results suggest that endoglin is an important mediator in the final common pathway of CKD and could be used as a possible new therapeutic target to counteract the progression towards end-stage renal disease (ESRD).
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