Nazari Alireza, Khorramdelazad Hossein, Hassanshahi Gholamhossein, Day Andrew S, Sardoo Atlas Mashayekhi, Fard Elnaz Tahmooresi, Abedinzadeh Mehdi, Nadimi Ali Esmaeili
Department of Surgery, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Molecular Medicine Research Center, Rafsanjan University of Medical Science, Rafsanjan, Iran; Department of Immunology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Life Sci. 2017 Dec 15;191:253-258. doi: 10.1016/j.lfs.2017.10.036.
Expression of S100A12, a small calcium-binding protein, by neutrophils and monocytes/macrophages induces proinflammatory responses via ligation with the receptor for advanced glycation end-products (RAGE) and subsequent activation of intracellular signal transduction pathways such as the nuclear factor (NF)-κB pathway. Although S100A12 has been demonstrated to be a useful biomarker during inflammatory conditions, its precise role in the pathogenesis of renal and cardiovascular diseases has not been fully understood. Recently, several studies have employed S100A12 transgenic mice to investigate its pathological effects. Further studies using these models are required before we can translate these findings to human diseases such as renal and cardiovascular diseases.
中性粒细胞和单核细胞/巨噬细胞表达的一种小的钙结合蛋白S100A12，通过与晚期糖基化终产物受体（RAGE）结合并随后激活细胞内信号转导通路（如核因子（NF）-κB通路）诱导促炎反应。尽管S100A12已被证明是炎症状态下一种有用的生物标志物，但其在肾脏和心血管疾病发病机制中的精确作用尚未完全明确。最近，几项研究采用S100A12转基因小鼠来研究其病理效应。在我们能够将这些发现转化应用于肾脏和心血管疾病等人类疾病之前，还需要使用这些模型进行进一步研究。
