Role of metastasis-induced protein S100A4 in human non-tumor pathophysiologies.
Role of metastasis-induced protein S100A4 in human non-tumor pathophysiologies.
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转移诱导蛋白 S100A4 在人类非肿瘤病理生理学中的作用
DOI：
10.1186/s13578-017-0191-1
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发表时间：
2017
影响因子：
7.5
通讯作者：
Zhang S
中科院分区：
文献类型：
--
作者：
Fei F;Qu J;Li C;Wang X;Li Y;Zhang S
S100A4是S100蛋白家族的重要成员，因其在促进肿瘤进展和转移中的重要作用而广为人知。除了在肿瘤中的表达外，S100A4的表达上调还与多种非肿瘤的病理生理过程有关。然而，S100A4的作用机制尚不清楚。在各种非肿瘤人类疾病中，激活的宿主细胞(成纤维细胞、免疫细胞、血管细胞等)分泌S100A4到细胞外空间，在那里它通过与细胞内靶蛋白相互作用来执行其生物学功能。然而，在不同的非肿瘤病理生理中，这些相互作用的确切分子机制是不同的，S100A4可能是作为生物机制共同内在成分的交联物之一。大量研究表明，S100A4介导的上皮-间充质转化在多种非肿瘤病理生理过程中起着至关重要的作用。根据输出细胞的表型和功能， 可以将 将 分为 、 三种一般亚型。S100A4通过多种信号通路调节与II型上皮-间充质转化相关的组织纤维化。此外，S100A4刺激成纤维细胞分泌纤维连接蛋白和胶原，从而形成细胞外基质(ECM)的结构成分，并刺激它们在组织中沉积，有助于形成促炎利基。同时，S100A4可增强巨噬细胞、中性粒细胞和白细胞的运动能力，促进这些炎性细胞的募集和趋化，从而调节炎症和免疫功能。S100A4还通过将神经元从脑损伤中拯救出来，对神经元起到神经保护促进生存的作用，并通过与其他靶分子相互作用参与血管生成。本文综述了S100A4在纤维化、炎症、免疫反应、神经保护、血管生成和一些常见的非肿瘤疾病中的作用，以及它可能参与的分子途径和潜在的临床价值。
S100A4, an important member of the S100 family of proteins, is best known for its significant role in promoting cancer progression and metastasis. In addition to its expression in tumors, upregulation of S100A4 expression has been associated with various non-tumor pathophysiology processes. However, the mechanisms underlying the role of S100A4 remain unclear. Activated “host” cells (fibroblasts, immunocytes, vascular cells, among others) secrete S100A4 into the extracellular space in various non-tumor human disorders, where it executes its biological functions by interacting with intracellular target proteins. However, the exact molecular mechanisms underlying these interactions in different non-tumor pathophysiologies vary, and S100A4 is likely one of the cross-linking factors that acts as common intrinsic constituents of biological mechanisms. Numerous studies have indicated that the S100A4-mediated epithelial–mesenchymal transition plays a vital role in the occurrence and development of various non-tumor pathophysiologies. Epithelial–mesenchymal transition can be categorized into three general subtypes based on the phenotype and function of the output cells. S100A4 regulates tissue fibrosis associated with the type II epithelial–mesenchymal transition via various signaling pathways. Additionally, S100A4 stimulates fibroblasts to secrete fibronectin and collagen, thus forming the structural components of the extracellular matrix (ECM) and stimulating their deposition in tissues, contributing to the formation of a pro-inflammatory niche. Simultaneously, S100A4 enhances the motility of macrophages, neutrophils, and leukocytes and promotes the recruitment and chemotaxis of these inflammatory cells to regulate inflammation and immune functions. S100A4 also exerts a neuroprotective pro-survival effect on neurons by rescuing them from brain injury and participates in angiogenesis by interacting with other target molecules. In this review, we summarize the role of S100A4 in fibrosis, inflammation, immune response, neuroprotection, angiogenesis, and some common non-tumor diseases as well as its possible involvement in molecular pathways and potential clinical value.
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影响因子：
5.5
作者：
Cerezo, Lucie Andres;Kuncova, Klara;Senolt, Ladislav
通讯作者：
Senolt, Ladislav
影响因子：
8
作者：
Ambartsumian, N;Klingelhöfer, J;Lukanidin, E
通讯作者：
Lukanidin, E
影响因子：
19.6
作者：
ALPERS, CE;SEIFERT, RA;BOWENPOPE, DF
通讯作者：
BOWENPOPE, DF
影响因子：
20.1
作者：
Brisset, Anne C.;Hao, Hiroyuki;Bochaton-Piallat, Marie-Luce
通讯作者：
Bochaton-Piallat, Marie-Luce
影响因子：
5
作者：
Doroudgar S;Quijada P;Konstandin M;Ilves K;Broughton K;Khalafalla FG;Casillas A;Nguyen K;Gude N;Toko H;Ornelas L;Thuerauf DJ;Glembotski CC;Sussman MA;Völkers M
通讯作者：
Völkers M