| Autor: |
Liu, Jing, Huang, Yan, Gong, Yiyi, Liu, Qingmei, Lin, Jinran, Liu, Jianlan, Liu, Mengguo, Huang, Jia, Pu, Weilin, Ma, Yanyun, Zhang, Yuting, Li, Haiyang, Shi, Xiangguang, Zhang, Yue, Wang, Jian, Zhu, Yifei, Wang, Qin, Wei, Kelu, Wang, Jiayi, Sha, Yu'ou |
| Předmět: |
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| Zdroj: |
Clinical & Translational Medicine; Dec2022, Vol. 12 Issue 12, p1-7, 7p |
| Abstrakt: |
Dear Editor, Fibrosis is characterized by fibroblast dysfunction and excessive deposition of cell-matrix that affect the normal functioning of the original tissue or organ.[1] The pathogenesis of keloids is complex and remains elusive. Fibroblasts interacted with endothelial cells via I ACKR1 i , while multiple chemokines ( I CXCL2 i , I CCL3L3 i ) secreted by myeloid cells interacted with I DPP4 i in fibroblasts (Figure 4D). (F) Interaction of macrophages and fibroblasts based on molecular patterns indicated that macrophages interact with fibroblasts via SPP1. CTHRC1+ fibroblasts are stimulated by macrophage-secreted SPP1 to induce excessive collagen deposition in keloids. [Extracted from the article] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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