In vivo molecular biological analysis proved that DDR1 activation exacerbates IPF inflammation through inflammasome signaling, macrophage activation, and M1/M2 polarization.

Apr 26, 2016 · The results suggested the discoidin domain receptor 1 (DDR1) and downstream c-Jun N-terminal kinases (JNK) pathway may play important roles in the progression of IPF.

Nov 24, 2021 · In this study we designed and synthesized a new indazole derivative XBLJ-13, and identified XBLJ-13 as a highly specific and potent DDRs inhibitor with anti-inflammation and anti-fibrosis...

Mar 15, 2024 · The discovery of compound 9 and its derivatives provides a promising core structure for the development of small molecule DDR1 inhibitors for the therapy of IPF.

As collagen deposition represents a key feature in fibrosis, the receptor tyrosine kinase Discoidin Domain Receptor1 (DDR1), which interacts and gets activated by collagens, was studied in IPF.

Dec 1, 2022 · It was confirmed in our research that of DDR1 signaling mainly located in macrophages to mediate inflammasome activation and macrophage polarization in IPF. Both specific DDR1 inhibitors DDR1-IN-1 and DDR1-IN-2 exerted significant anti-inflammatory and anti-fibrotic effects in IPF.

In IPF patients, DDR1 activation in fibroblasts inhibited Fas ligand-induced apoptosis and resulted in NF-kappaB nuclear translocation. Suppression of DDR1 expression in fibroblasts by siRNA abolished these effects, and an NF-kappaB inhibitor abrogated the anti-apoptotic effect of …

Nov 2, 2022 · In this research, we developed a high-hit rate, effective screening method that serves as a theoretical guide for finding DDR1 inhibitors for the development of IPF therapeutics.

Oct 1, 2018 · The EP300 siRNA and inhibitors sensitized DDR1 inhibitors in pulmonary fibrosis models in vitro and in vivo, implicating a combined inhibition of DDR1 with EP300 as potential therapies for IPF.

In this study, we examined in vivo and in vitro DDR1 expression and its role in cell survival using fibroblasts obtained from IPF and non-IPF patients. Immunohistochemically, fibroblasts present in fibroblastic foci expressed endogenous DDR1.