Lay A TRAP for myeloid cell response in diabetic kidney disease
Lay A TRAP for myeloid cell response in diabetic kidney disease
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为糖尿病肾病的骨髓细胞反应设置陷阱
DOI：
10.1016/j.kint.2022.02.001
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发表时间：
2022
影响因子：
19.6
通讯作者：
Hiroshi Nishi
中科院分区：
文献类型：
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作者：
Wada T;Akiyama S;他41名;Hiroshi Nishi
肾素-血管紧张素系统的功能在糖尿病肾病的进展中至关重要。ATRAP是一种1型血管紧张素II受体相关蛋白，负调节细胞内血管紧张素II信号传导。在这个问题上，Haruharaet al.揭示了糖尿病小鼠ATRAP缺陷减少抗炎巨噬细胞浸润并加剧蛋白尿。ATRAP的过继转移和肾小管特异性耗竭突出了肾小球损伤与肾小管间质血管紧张素II信号传导和先天免疫之间的串扰。
The functions of the renin-angiotensin system are crucial in the progression of diabetic kidney disease. ATRAP is a type 1 angiotensin II receptor–associated protein that negatively regulates intracellular angiotensin II signaling. In this issue, Haruharaet al.revealed that ATRAP deficiency of diabetic mice decreases anti-inflammatory macrophage infiltration and exacerbates albuminuria. The adoptive transfer and tubule-specific depletion of ATRAP highlight the crosstalk between glomerular injury and tubulointerstitial angiotensin II signaling and innate immunity.