Disruption of Kidney-Immune System Crosstalk in Sepsis with Acute Kidney Injury: Lessons Learned from Animal Models and Their Application to Human Health

被引:23
作者
LaFavers, Kaice [1 ]
机构
[1] Indiana Univ Sch Med, Div Nephrol & Hypertens, Dept Med, Evansville, IN 47708 USA
关键词
sepsis; acute kidney injury; immune crosstalk; erythropoietin; vitamin D; uromodulin; AUTOPHAGY CONTRIBUTES; URINARY UROMODULIN; OXIDATIVE STRESS; SERUM UROMODULIN; SEPTIC SHOCK; NITRIC-OXIDE; ERYTHROPOIETIN; DYSFUNCTION; ACTIVATION; MONOCYTES;
D O I
10.3390/ijms23031702
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In addition to being a leading cause of morbidity and mortality worldwide, sepsis is also the most common cause of acute kidney injury (AKI). When sepsis leads to the development of AKI, mortality increases dramatically. Since the cardinal feature of sepsis is a dysregulated host response to infection, a disruption of kidney-immune crosstalk is likely to be contributing to worsening prognosis in sepsis with acute kidney injury. Since immune-mediated injury to the kidney could disrupt its protein manufacturing capacity, an investigation of molecules mediating this crosstalk not only helps us understand the sepsis immune response, but also suggests that their supplementation could have a therapeutic effect. Erythropoietin, vitamin D and uromodulin are known to mediate kidney-immune crosstalk and their disrupted production could impact morbidity and mortality in sepsis with acute kidney injury.
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收藏
页数:16
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