Putative regulation of macrophage-mediated inflammation by catestatin.
Putative regulation of macrophage-mediated inflammation by catestatin.
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DOI：
10.1016/j.it.2021.11.002
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发表时间：
2021-11
影响因子：
16.8
通讯作者：
Elke M. Muntjewerff;G. Christoffersson;S. Mahata;Geert van den Bogaart
中科院分区：
文献类型：
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作者：
Elke M. Muntjewerff;G. Christoffersson;S. Mahata;Geert van den Bogaart
Catestatin（CST）是神经内分泌前体嗜铬粒蛋白A（CgA）的生物活性裂解产物。最近的研究表明，CST可以发挥抗炎和抗肾上腺素能的作用，通过抑制哺乳动物巨噬细胞的炎症反应。然而，最近的研究结果也表明，巨噬细胞本身是主要的CST生产者。在此，我们假设巨噬细胞以炎症依赖性方式产生CST，从而可能以自分泌方式自我调节炎症。CST与以慢性炎症为特征的病理状况相关，包括自身免疫性疾病、心血管疾病和代谢疾病。由于在糖尿病和炎症性肠病的小鼠模型中腹腔注射CST已被报道有益于减轻疾病，我们认为CST应作为治疗某些炎症性疾病的候选靶点进行进一步研究。
Catestatin (CST) is a bioactive cleavage product of the neuroendocrine prohormonechromogranin A(CgA). Recent findings show that CST can exert anti-inflammatory and antiadrenergic effects by suppressing the inflammatory actions of mammalian macrophages. However, recent findings also suggest that macrophages themselves are major CST producers. Here, we hypothesize that macrophages produce CST in an inflammation-dependent manner and thereby might self-regulate inflammation in an autocrine fashion. CST is associated with pathological conditions hallmarked by chronic inflammation, including autoimmune, cardiovascular, and metabolic disorders. Since intraperitoneal injection of CST in mouse models of diabetes and inflammatory bowel disease has been reported to be beneficial for mitigating disease, we posit that CST should be further investigated as a candidate target for treating certain inflammatory diseases.