TY  - JOUR
A1  - Sarakpi, Tamim
A1  - Mesic, Armir
A1  - Speer, Thimoteus
T1  - Leukocyte–endothelial interaction in CKD
T2  - Clinical kidney journal
N2  - Chronic kidney disease (CKD) represents an independent risk factor for cardiovascular diseases (CVD). Accordingly, CKD patients show a substantial increased risk of cardiovascular mortality. Inflammation represents an important link between CKD and CVD. The interaction between endothelial cells and effector cells of the innate immune system plays a central role in the development and progression of inflammation. Vascular injury causes endothelial dysfunction, leading to augmented oxidative stress, increased expression of leukocyte adhesion molecules and chronic inflammation. CKD induces numerous metabolic changes, creating a uremic milieu resulting in the accumulation of various uremic toxins. These toxins lead to vascular injury, endothelial dysfunction and activation of the innate immune system. Recent studies describe CKD-dependent changes in monocytes that promote endothelial dysfunction and thus CKD progression and CKD-associated CVD. The NLR family pyrin domain containing 3–interleukin-1β–interleukin-6 (NLRP3–IL-1β–IL-6) signaling pathway plays a pivotal role in the development and progression of CVD and CKD alike. Several clinical trials are investigating targeted inhibition of this pathway indicating that anti-inflammatory therapeutic strategies may emerge as novel approaches in patients at high cardiovascular risk and nonresolving inflammation. CKD patients in particular would benefit from targeted anti-inflammatory therapy, since conventional therapeutic regimens have limited efficacy in this population.
KW  - adhesion
KW  - cardiovascular disease
KW  - chronic kidney disease
KW  - inflammation
Y1  - 2023
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/83483
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-834832
SN  - 2048-8505
VL  - 16
IS  - 11
SP  - 1845
EP  - 1860
PB  - Oxford University Press
CY  - Oxford
ER  -