Regulations of TLR4 and TLR9 signals in macrophages by Lumican. Synthesized de novo by activated fibroblasts or released in the tissue microenvironment from a remodeling ECM, lumican enhances TLR4 and restricts TLR9 signals in macrophages.

2020年1月15日 · Fibronectin is an extracellular matrix (ECM) protein which is polymerized by adherent cells into a mechanically sensitive network of interacting fibers. Fibronectin is up-regulated in the stroma of solid tumors and has been shown to contribute to cancer cell growth, migration, invasion, survival and resistance to chemotherapy [2,3].

Here we review the role of extracellular matrix (ECM)-derived DAMPS in the activation of TLR4 signaling in the context of tumor progression. We also explore the various types of topographical changes that can lead to ECM-derived DAMPs and their contribution to TLR4 activation.

2025年3月21日 · Additionally, signaling associated with vascular development and ECM stability—such as Vegfd-Vegfr3, Vegfd-Vegfr2r3, Tgfb1-(Tgfbr1+Tgfbr2), and Selplg-Selp—was more prominent in the Tlr4-/-CLP ...

2024年2月7日 · We show that TLR4 influences inflammation, cell death, and ECM deposition at late-stage post-injury when secondary injury processes are normally considered to be over. This highlights the potential for late-stage targeting of TLR4 as a potential therapy for chronic SCI.

2023年3月17日 · In Tlr4 −/− mice transplanted with WT BM, the pharmacological inhibition of TLR4 signaling with TAK-242 demonstrated significantly higher ECM accumulation and downregulation of hepatic MMP12 (Figures 3 C and 3E). Ly6C expression and frequency in CD11b + macrophages did not change in both chimeras (Figures S4 B …

2018年7月12日 · Endogenous TLR4 ligand DAMPs include ECM proteins such as hyaluronan, fibrinogen, tenascin-C, and fibronectin-EDA that are generated within injured microenvironments, where they function as danger signals or alarmins enabling both hematopoietic and tissue-resident cells to sense and respond to damage.

2025年1月31日 · Artesunate has been reported to inhibit the Toll-like receptor 4 (TLR4) pathway in macrophages after stimulation with lipopolysaccharide (LPS), which explains artesunate’s protective effect in ...

我们发现，当继发性损伤过程通常被认为已经结束时，tlr4 会影响损伤后后期的炎症、细胞死亡和 ecm 沉积。 这凸显了 TLR4 后期靶向作为慢性 SCI 潜在疗法的潜力。

The results of the present study suggest that control of TLR4 activity or modulation of TLR4 signaling can suppress the inflammatory responses and ECM protein remodeling in the remote non-ischemic myocardium after myocardial I/R injury.