The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD.
The Signaling Pathway of TNF Receptors: Linking Animal Models of Renal Disease to Human CKD.
复制标题
肿瘤坏死因子受体的信号通路:将肾脏疾病动物模型与人类慢性肾脏病联系起来。
DOI:
10.3390/ijms23063284
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发表时间:
2022-03-18
影响因子:
5.6
通讯作者:
Belo L
中科院分区:
文献类型:
--
作者:
Lousa I;Reis F;Santos-Silva A;Belo L
Chronic kidney disease (CKD) has been recognized as a global public health problem. Despite the current advances in medicine, CKD-associated morbidity and mortality remain unacceptably high. Several studies have highlighted the contribution of inflammation and inflammatory mediators to the development and/or progression of CKD, such as tumor necrosis factor (TNF)-related biomarkers. The inflammation pathway driven by TNF-α, through TNF receptors 1 (TNFR1) and 2 (TNFR2), involves important mediators in the pathogenesis of CKD. Circulating levels of TNFRs were associated with changes in other biomarkers of kidney function and injury, and were described as predictors of disease progression, cardiovascular morbidity, and mortality in several cohorts of patients. Experimental studies describe the possible downstream signaling pathways induced upon TNFR activation and the resulting biological responses. This review will focus on the available data on TNFR1 and TNFR2, and illustrates their contributions to the pathophysiology of kidney diseases, their cellular and molecular roles, as well as their potential as CKD biomarkers. The emerging evidence shows that TNF receptors could act as biomarkers of renal damage and as mediators of the disease. Furthermore, it has been suggested that these biomarkers could significantly improve the discrimination of clinical CKD prognostic models.
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影响因子:
16
作者:
Ea, CK;Deng, L;Chen, ZJJ
通讯作者:
Chen, ZJJ
影响因子:
2.5
作者:
An, Jung Nam;Yoo, Kyung Don;Lee, Jung Pyo
通讯作者:
Lee, Jung Pyo
影响因子:
5.5
作者:
Bartolucci, P;Ramanoelina, J;Guillevin, L
通讯作者:
Guillevin, L
影响因子:
5.8
作者:
Borghi, Alice;Haegman, Mira;Beyaert, Rudi
通讯作者:
Beyaert, Rudi
影响因子:
3.8
作者:
DEMBIC Z;LOETSCHER H;LESSLAUER W
通讯作者:
LESSLAUER W