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Purpose Investigate the mechanism of how sodium butyrate (NaBut) improves mitochondrial function and kidney tissue injury in diabetic kidney disease (DKD) via the AMPK/PGC-1α pathway.Methods Assess the effects of NaBut on glucose and insulin tolerance, urine, and gut microbial composition in db/db and db/m mice. Use flow cytometry and western blotting to detect the effects of NaBut on apoptosis, kidney mitochondrial function, and AMPK/PGC-1α signaling. Use HK-2 cells induced by high glucose (HG) to establish the DKD model in vitro and detect changes in the AMPK/PGC-1α signaling pathway and mitochondrial function after NaBut intervention.Results NaBut attenuated blood glucose levels and reversed increases in urine and serum levels of glucose, BUN, Ucr, TG, TC, and UAE in db/db mice. NaBut improved insulin tolerance, reversed PGC-1α and p-AMPK expression level in the kidneys of db/db mice, and improved lipid accumulation and mitochondrial function. NaBut was able to reverse the effects of elevated glucose, compound C, and siRNA-PGC on ROS and ATP levels. Additionally, it increased protein expression of PGC-1α and p-AMPK.Conclusion NaBut activates the kidney mitochondrial AMPK/PGC-1α signaling pathway and improves mitochondrial dysfunction in DKD, thus protecting kidney tissue in vitro and in vivo.

The continuous accumulation of extracellular matrix will eventually lead to glomerular sclerosis, interstitial fibrosis, tubular atrophy and vascular sclerosis, which are involved in the progression of chronic kidney disease (CKD). If these processes can be discovered early and effective interventions given in time, the progression of kidney disease may be delayed. Therefore, exploring new biomarkers and therapeutic targets that can identify CKD at an early stage is urgently needed. In recent years, studies have shown that urine periostin may be used as a marker of early renal tubular injury. And in an animal model experiment of hypertensive nephropathy, periostin is involved in the progression of kidney injury and reflects its progression. Here we review the current progress on the role of periostin in pathologic pathways of kidney system to explore whether periostin is a potential therapeutic target for the treatment of CKD.

We aimed to investigate the effect of As2O3 treatment on Wnt/β-catenin signaling pathway-related genes and pathways in renal cancer. Illumina-based RNA-seq of 786-O cells with or without As2O3 treatment was performed, and differentially expressed genes (DEGs) were identified using Cuffdiff software. TargetMine was utilized to perform Gene Ontology (GO) pathway and Disease Ontology enrichment analyses. Furthermore, TRANSFAC database and LPIA method were applied to select differentially expressed transcription factors (TFs) and pathways related to Wnt/β-catenin signaling pathway, respectively. Additionally, transcriptional regulatory and pathway crosstalk networks were constructed. In total, 1684 DEGs and 69 TFs were screened out. The 821 up-regulated DEGs were mainly enriched in 67 pathways, 70 GO terms, and 46 disease pathways, while only 1 pathway and 5 GO terms were enriched for 863 down-regulated DEGs. A total of 18 DEGs (4 up-regulated and 14 down-regulated genes) were involved in the Wnt/β-catenin signaling pathway. Among the 18 DEGs, 4 ones were TFs. Furthermore, 211 pathways were predicted to be linked to the Wnt/β-catenin signaling pathway. In conclusion, As2O3 may have a significant effect on the Wnt/β-catenin signaling pathway for renal cancer treatment. The potential key DEGs are expected to be used as therapeutic targets.