Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.
J, N., S, F., M, Q., H, Z., & Y, C. (2026). Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.. Inflammation research : official journal of the European Histamine Research Society ... [et al.]. https://doi.org/10.1007/s00011-026-02339-x
J N, S F, M Q, H Z, Y C. Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.. Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 2026; doi: 10.1007/s00011-026-02339-x
J N, S F, M Q, et al. Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.[J]. Inflammation research : official journal of the European Histamine Research Society ... [et al.]. 2026. DOI: 10.1007/s00011-026-02339-x.
@article{j2026,
author = {Ning J and Fang S and Qiu M and Zou H and Chen Y},
title = {Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.},
journal = {Inflammation research : official journal of the European Histamine Research Society ... [et al.]},
year = {2026},
doi = {10.1007/s00011-026-02339-x},
note = {PMID: 42608597},
}
TY - JOUR AU - Ning J AU - Fang S AU - Qiu M AU - Zou H AU - Chen Y TI - Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease. T2 - Inflammation research : official journal of the European Histamine Research Society ... [et al.] PY - 2026 DO - 10.1007/s00011-026-02339-x AN - PMID:42608597 ER -
BACKGROUND: High phosphate levels lead to significant pathological changes in vascular smooth muscle cells (VSMCs) and endothelial cells, driving vascular disease in chronic kidney disease (CKD). Endothelial cell senescence plays a major role in this process, promoting vascular calcification by fostering a pro-inflammatory and pro-osteogenic environment. Interaction between VSMCs and endothelial cells further accelerates calcification, although the precise mechanisms remain incompletely understood. METHODS: Exosomes were isolated and characterized, with RT-qPCR, western blot, immunohistochemistry (IHC), and immunofluorescence (IF) assays used to confirm gene and protein expression. Chromatin immunoprecipitation (ChIP) and dual-luciferase assays were conducted to assess interactions between BACH1 and COL3A1. A 5/6 nephrectomy-induced CKD mouse model was established, and Alizarin Red S staining, Von Kossa staining, calcium content measurement, and ALP activity assays were performed to assess vascular calcification and osteogenic differentiation. RESULTS: Knocking down BACH1 reduced high phosphate-induced senescence in endothelial cells and suppressed TNF-α-induced EndMT in these cells. BACH1 also enhanced COL3A1 expression by activating its transcription. Endothelial cell-derived COL3A1 was associated with exosomes, and HAoEC-derived exosomes were internalized by VSMCs, thereby promoting calcification-related phenotypes in VSMCs. In vivo, systemic COL3A1 knockdown attenuated CKD-associated vascular calcification, EndMT-like changes, and senescence. CONCLUSION: In summary, BACH1 regulates COL3A1, facilitating communication between endothelial cells and VSMCs through exosomes, thereby promoting vascular calcification in CKD. These findings highlight that targeting the BACH1-COL3A1 axis and exosome-mediated endothelial-VSMC communication may represent a potential therapeutic strategy.