Growth differentiation factor-15 (GDF15), leucine-rich alpha-2-glycoprotein 1 (LRG1), and secreted phosphoprotein 1 (SPP1/ osteopontin, OPN) were identified as potential candidate markers by proteomic analysis and were validated by ELISA in another 30 patients and in a CP-induced AKI mouse model.
Additionally, although MAP3K7 (MEKK7, TAK1) is required for kidney development, acutely targeting MAP3K7 protected from acute and chronic kidney injury; and targeting MAP3K8 (TPL2/Cot) protected from acute kidney injury.
Furthermore, inhibition of CXCR2 by intragastric administration of repertaxin in mice with AKI reduces kidney injury associated with a reduction of inflammatory cytokines and neutrophils infiltration.
Global microRNA(miRNA) expression profiling of renal exosomes was examined in a LPS induced acute kidney injury (AKI) mouse model and miR-19b-3p was identified as the miRNA that was most notably increased in TEC-derived exosomes compared to controls.
The cytokine interleukin 34 (IL-34) enhances proliferation and differentiation of myeloid cells and secretion of pro-inflammatory cytokines, which is involved in the pathogenesis of some inflammatory and infectious diseases, including acute kidney injury.
The pathogenesis of AKI in sepsis is incompletely understood.In this issue of the JCI, Hato et al. investigate the renal translatome during bacterial sepsis and identify the global shutdown of renal protein translation mediated by the eukaryotic translation initiation factor 2-α kinase 2/eukaryotic translation initiation factor 2α (EIF2AK2/eIF2α) axis as a major pathway in mediating septic AKI.
In summary, our study provides experimental evidence showing that RORα is a novel endogenous protector against renal I/R injury and that ROR-α activation is a promising therapeutic strategy for the prevention of acute kidney injury.-Cai, J., Jiao, X., Fang, Y., Yu, X., Ding, X.
Risks of AKI (OR = 0.47, 95% CI 0.27-0.80), hospitalization (OR = 0.66, 95% CI 0.56-0.78) or all-cause mortality (OR = 0.43, 95% CI 0.20-0.95) were lower in patients initiating SGLT2-i versus DPP-4i.
Together, our results identify a key role for TMEM33 in the regulation of intracellular calcium homeostasis of renal proximal convoluted tubule cells and establish a causal link between TMEM33 and acute kidney injury.
We have previously reported that the protein thrombospondin-1 and its receptor CD47 are induced in AKI; however, the mechanism underlying their regulation of injury is unknown.
Gal-3-dependent nephroprotective and immunosuppressive effects of renal DCs was due to the IDO1-induced expansion of renal Tregs since either inhibition of IDO1 activity in TLR-2-primed DCs or depletion of Tregs completely diminished DCs-mediated attenuation of CDDP-induced AKI.
Hyperchloremia is common in patients with AP and Δ[Cl<sup>-</sup>] and chloride exposure during the first 48 h were independent risk factors for AKI in MSAP and SAP patients.
We demonstrated that miR-155 exacerbated AKI involving the targeting and regulation of TCF4/Wnt/β-catenin signaling pathway, indicating a novel regulatory network and elucidating a potential target for IRI-induced AKI treatment.