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Initiation of the inflammatory response after renal ischemia/reperfusion injury during renal transplantation

  • Nephrology - Review
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Abstract

Ischemia/reperfusion injury (IRI) occurs commonly during renal transplantation. It has been well demonstrated that the inflammatory response has an important role in the pathogenesis and pathological processes of IRI. However, the signaling events that trigger the activation of the inflammatory response are less clear. Accumulated evidence has identified the role of various injury factors released from or exposed in ischemic, damaged, or dying cells, which serve as initiators of the inflammatory response and exacerbate kidney injury after renal IRI. Signaling pathways triggered by these endogenous molecules that activate different pathogen recognition receptors have also been widely investigated. Here, we review the molecular signaling molecules that initiate the inflammatory response during renal IRI and that provide potential therapeutic options for the disease.

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Abbreviations

AKI:

Acute kidney injury

ASC:

Apoptosis associated speck-like protein containing a caspase recruitment domain

BUN:

Blood urea nitrogen

DAMPs:

Damage associated molecular patterns

DAP:

Daphnetin

DKO:

Double knockout

Gly:

Glycyrrhizin

HMGB1:

High-mobility group box 1

HSPs:

Heat shock proteins

IKK:

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor Kinase

IL:

Interleukin

IRAK:

IL-1 receptor associated kinase

IRI:

Ischaemia/reperfusion injury

LRR:

Leucine-rich repeat

MBL:

Mannan-binding lectin

MyD88:

Myeloid differentiation protein 88

NLAP:

Neutrophilic alkaline phosphatase

NLRs:

Nucleotide binding and oligomerization domain (NOD)-like receptors

NLRP3:

Nod-like receptors, the pyrin domain containing protein 3

NF-κB:

Nuclear factor kappa-light-chain-enhancer of activated B cells

PAMPs:

Pathogen-associated molecular patterns

PRRs:

Pathogen recognition receptors

P2RX7:

Purinergic receptor P2X, ligand-gated ion channel, 7

ROS:

Reactive oxygen species

RTECs:

Renal tubular epithelial cells

TECs:

Tubular epithelial cells

TLRs:

Toll-like receptors

TRAM:

TRIF-related adaptor molecule

TRAF6:

Tumor necrosis factor receptor-associated factor 6

TRIF:

TIR domain-containing adapter inducing IFNβ

TNF-α:

Tumor necrosis factor

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Acknowledgements

This work was supported by the National Natural Science Foundation of China (Nos. 81771283, 81301019 to Lijuan Gu, No. 81571147 to Xiaoxing Xiong and No. 21708012 to Yao Sun). We thank Ann Turnley, PhD, from Li wen Bian ji, Edanz Group China (http://www.liwenbianji.cn/ac), for editing the English text of a draft of this manuscript.

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Gu, L., Tao, Y., Chen, C. et al. Initiation of the inflammatory response after renal ischemia/reperfusion injury during renal transplantation. Int Urol Nephrol 50, 2027–2035 (2018). https://doi.org/10.1007/s11255-018-1918-6

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