红细胞分布宽度(red cell distribution width,RDW)是通过定量的方法反映循环中红细胞大小变异性的指标。近期较多研究发现RDW的升高能够作为预测人群心血管疾病预后不良的指标,即使RDW值在正常参考值范围内,处于高值的人群存在更高的心血管疾病死亡风险。本文综述了RDW与高血压发病、血压水平、血压形态及靶器官损害之间的关系,并探讨了RDW升高提示高血压预后不良的机制。由于RDW简单易得,可以作为高血压患者预后风险评估有潜力的指标。
Objective Tacrolimus （FK506） is an immunosuppressive drug, which is widely used to prevent rejection of transplanted organs. However, chronic administration of FK506 leads to hypertension in solid organ transplantation patients, and its molecular mechanisms are much more complicated. In this review, we will discuss the above-mentioned molecular mechanisms of FK506-induced hypertension in solid organ transplantation subjects. Data sources The data analyzed in this review were mainly from relevant articles without restriction on the publication date reported in PubMed. The terms ＂FK506＂ or ＂tacrolimus＂ and ＂hypertension＂were used for the literature search. Study selection Original articles with no limitation of research design and critical reviews containing data relevant to FK506-induced hypertension and its molecular mechanisms were retrieved, reviewed and analyzed. Results There are several molecular mechanisms attributed to FK506-induced hypertension in solid organ transplantation subjects. First, FK506 binds FK506 binding protein 12 and its related isoform 12.6 （FKBP12/12.6） and removes them from intracellular ryanodine receptors that induce a calcium ion leakage from the endoplasmic/sarcoplasmic reticulum. The conventional protein kinase C beta II （cPKCI311）-mediated phosphorylation of endothelial nitric oxide （NO） synthase at Thr495, which reduces the production of NO, was activated by calcium ion leakage. Second, transforming growth factor receptodSMAD2/3 signaling activation plays an important role in Treg/Th17 cell imbalance in T cells which toget converge to cause inflammation, endothelial dysfunction, and hypertension following tacrolimus treatment. Third, the activation of with-no-K（Lys） kinases/STE20/SPSl-related proline/alanine-rich kinase/thiazide-sensitive sodium chloride co-transporter （WNKs/SPAK/NCC） pathway has a central role in tacrolimus-induced hypertension. Finally, the enhanced activity of renal renin-angiotensin-aldosterone system seems to play a crucial
Wang Jianglin Guo Ren Liu Shikun Chen Qingjie Zuo Shanru gang Meng Zuo Xiaocong
