TLR9 deletion reduced vascular calcification in ApoE-deficient mice, as evidenced by von Kossa staining (5.83% vs. 3.04%; P < 0.05) and decreased BMP-2 expression.
Does genetic deletion of TLR9 reduce vascular calcification and chondrogenesis in ApoE-/- mice?
TLR9 signaling promotes vascular calcification and chondrogenesis via macrophage-driven upregulation of BMP-2 and RANKL, suggesting TLR9 as a potential therapeutic target for vascular calcification.
Absolute Event Rate: 0% vs 0%
Vascular calcification represents a significant clinical challenge, leading to cardiovascular disease, though its underlying mechanisms remain incompletely understood. Recent studies indicate that Toll-like receptor 9 (TLR9), a key element of innate immunity, plays a pathogenic role in vascular inflammation and atherogenesis. Therefore, we hypothesized that TLR9 signaling promotes vascular chondrogenesis and calcification. We compared apolipoprotein E-deficient (ApoE-/-) mice and Tlr9-/- ApoE-/- mice after 24 -weeks high-cholesterol diet feeding. There were no differences between the groups in body weight gain, blood pressure, or plasma glucose levels, although total cholesterol levels were significantly lower in the Tlr9-/- ApoE-/- mice. The genetic deletion of TLR9 attenuated vascular calcification as determined by von Kossa staining (5.83 ± 1.14% vs. 3.04 ± 0.68%; P -/- mice. Our analyses suggest that TLR9 pathway contributes to bone morphogenic activation of macrophages and VSMCs at least partially, participating in the development of vascular calcification.
Bando et al. (Mon,) reported a other. TLR9 deletion reduced vascular calcification in ApoE-deficient mice, as evidenced by von Kossa staining (5.83% vs. 3.04%; P < 0.05) and decreased BMP-2 expression.
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