KRT20 Suppresses Exosomal Secretion of PRDX2 and Ferroptosis in Acute Kidney Injury.

Background: Acute kidney injury (AKI) is a prevalent clinical syndrome with insufficient kidney function. Keratin 20 (KRT20), a component of intermediate filaments, is widely recognized as a biomarker of kidney tubular injury, yet its exact function in kidney disease remains uncertain.

Methods: RNA sequencing data from a mouse model of ischemia/reperfusion-induced AKI were analyzed to assess KRT20 transcript levels.

Molecular characterization and functional prioritization of CD46, IL6R, KLRC1, LEAP2 and SMOX as candidate targets in acute kidney injury.

Acute kidney injury (AKI) remains a critical condition with limited pharmacological options. Bioactive molecules, including cytokines, receptors, and enzymes, play central roles in AKI pathogenesis, but systematic efforts to identify translational targets remain limited. In this study, we implemented a multi-omics integrative framework to nominate and validate candidate targets for AKI.

Oxidative Stress: Signaling Pathways, Biological Functions, and Disease.

The dysregulated accumulation of reactive oxygen species (ROS) and reactive nitrogen species disrupts redox homeostasis, triggering oxidative stress (OS) and driving pathophysiological changes across multiple organ systems. OS modulates critical signaling pathways, induces inflammation, impairs mitochondrial function, alters metabolic homeostasis, and dysregulates autophagy, contributing to disease progression. While prior research has largely focused on OS within single-organ diseases (e.

Diagnostic value of hsa_circ_0012138 in the chronic progression of obstructive nephropathy.

Background: Obstructive nephropathy (ON) is caused by obstruction of urine flow, featured with progressive renal dysfunction and progressing into chronic kidney disease. There is still controversy whether to remove the kidney or simply relieve obstruction in patients with late diagnosis. Reliable biomarker is needed for predicting renal function reversibility in ON patients.

Investigation of potential toxicity associated with long-term amitriptyline exposure: Evidence from genomics.

The increasing environmental detection of antidepressants such as amitriptyline (AT) has raised toxicological concerns, yet its long-term safety profile remains poorly characterized. We applied an integrative strategy combining phenome-wide association studies (PheWAS), Mendelian randomization (MR), network toxicology, and molecular docking to systematically evaluate potential adverse effects of AT. PheWAS analyses were performed across 784 phenotypes using UK Biobank and FinnGen (R10).

Dissecting the role of metformin in urogenital malignancies.

Metformin has shown great potential for anti-tumor therapy according to laboratory results, but there is currently no consensus on the role it playing in the pathogenesis of urogenital malignancies. Initially, a systematic review was conducted on clinical research examining the association between the use of metformin and the incidence and prognosis of prevalent urogenital malignancies. Then, a retrospective analysis of the participants in NHANES was performed to strengthen the study.

Identification of druggable targets in acute kidney injury by proteome- and transcriptome-wide Mendelian randomization and bioinformatics analysis.

Background: Acute kidney injury (AKI) remains a critical condition with limited therapeutic options, predominantly managed by renal replacement therapy. The challenge of developing targeted treatments persists.

Methods: We integrated genetic data related to druggable proteins and gene expression with AKI genome-wide association study (GWAS) findings.

CAV1 Exacerbates Renal Tubular Epithelial Cell Senescence by Suppressing CaMKK2/AMPK-Mediated Autophagy.

Renal proximal tubular epithelial cell (PTEC) senescence and defective autophagy contribute to kidney aging, but the mechanisms remain unclear. Caveolin-1 (CAV1), a crucial component of cell membrane caveolae, regulates autophagy and is associated with cellular senescence. However, its specific role in kidney aging is poorly understood.

ACSL5 promotes lipid deposition and lipoapoptosis in proximal tubular epithelial cells of diabetic kidney disease.

Background: Lipoapoptosis in Proximal tubular epithelial cells (PTCs) are substantial in the etiology of diabetic kidney disease (DKD), yet the underlying mechanisms warrant further investigation. Acyl-CoA synthetase long-chain family member 5 (ACSL5) facilitates the formation of acyl-CoA, however, the precise role of ACSL5 in lipoapoptosis of PTCs in DKD remains inconclusive.

Methods: Transcriptomic data analysis identified the hub gene Acsl5 associated with lipid metabolism in DKD.

PRMT4 interacts with NCOA4 to inhibit ferritinophagy in cisplatin-induced acute kidney injury.

Cisplatin-induced acute kidney injury (AKI) is commonly seen in the clinical practice, and ferroptosis, a type of non-apoptotic cell death, plays a pivotal role in it. Previous studies suggested that protein arginine methyltransferase 4 (PRMT4) was incorporated in various bioprocesses, but its role in renal injuries has not been investigated. Our present study showed that PRMT4 was highly expressed in renal proximal tubular cells, and it was downregulated in cisplatin-induced AKI.

Identification of TACSTD2 as novel therapeutic targets for cisplatin-induced acute kidney injury by multi-omics data integration.

Cisplatin-induced acute kidney injury (CP-AKI) is a common complication in cancer patients. Although ferroptosis is believed to contribute to the progression of CP-AKI, its mechanisms remain incompletely understood. In this study, after initially processed individual omics datasets, we integrated multi-omics data to construct a ferroptosis network in the kidney, resulting in the identification of the key driver TACSTD2.

Exploration of the prognostic effect of costimulatory genes in bladder cancer.

Background: A prognostic model of bladder cancer was constructed based on costimulatory molecules, and its stability and accuracy were verified in different datasets.

Method: The expression profile of bladder cancer RNA and the corresponding clinical data in The Cancer Genome Atlas (TCGA) database were analyzed employing computational biology, and a prognostic model was constructed for costimulating molecule-related genes. The model was applied in GSE160693, GSE176307, Xiangya_Cohort, GSE13507, GSE19423, GSE31684, GSE32894, GSE48075, GSE69795 and GSE70691 in TCGA dataset and Gene Expression Omnibus database.

CHIP protects against septic acute kidney injury by inhibiting NLRP3-mediated pyroptosis.

Septic acute kidney injury (S-AKI), the most common type of acute kidney injury (AKI), is intimately related to pyroptosis and oxidative stress in its pathogenesis. Carboxy-terminus of Hsc70-interacting protein (CHIP), a U-box E3 ligase, modulates oxidative stress by degrading its targeted proteins. The role of CHIP in S-AKI and its relevance with pyroptosis have not been investigated.

WBP2 restrains the lysosomal degradation of GPX4 to inhibit ferroptosis in cisplatin-induced acute kidney injury.

Cisplatin is one of the major causes of acute kidney injury (AKI) in clinical practice, and ferroptosis is an essential form of cell death in cisplatin-induced AKI (CP-AKI). WW domain binding protein-2 (WBP2), a molecular chaperon, is involved in the progression of various malignancies, but its role in renal injuries has not been investigated. Our present study employed bioinformatics analysis to identify WBP2 as a potential modulator of AKI and ferroptosis.

Identification of RPS7 as the Biomarker of Ferroptosis in Acute Kidney Injury.

Objective: This paper aims to explore novel ferroptosis-related biomarkers for acute kidney injury (AKI).

Methods: Various bioinformatic methods, such as differential expression analysis, functional annotation analysis, machine learning, and chemical-gene network analysis, were used in this study. Furthermore, the expression and proferroptotic role of RPS7 were validated with further bioinformatics analysis and biochemical experiments.

Performance Enhancement of the Poplar Wood Composites Biomimetic Mineralized by CaCO.

Inspired by the natural matrix-mediated biomineralization, wood composites were prepared by vacuum impregnation using the gel effect of sodium alginate (SA) on calcium ions, which improved the mechanical properties, flame retardant, and smoke suppression properties of the wood composites. Fourier transform infrared spectroscopy (FTIR), X-ray diffraction (XRD) and scanning electron microscopy (SEM) confirmed that the SA inducer had promoted the orderly deposition and directional crystallization of calcium carbonate (CaCO) inside the wood cell walls and intercellular spaces. The density and weight gain rate of the biomimetic mineralized wood showed that CaCO effectively adhered to the interior of wood with SA as an inducer.

Cocaine detection using aptamer and molybdenum disulfide-gold nanoparticle-based sensors.

The current work highlighted a novel colorimetric sensor based on aptamer and molybdenum disulfide (MoS)-gold nanoparticles (AuNPs) that was developed for cocaine detection with high sensitivity. Due to the presence of the plasmon resonance band on the surface of AuNPs, AuNPs aggregated and the color was changed from red to blue after adding a certain concentration of NaCl. We used MoS to optimize the sensing system of AuNPs.

Highly sensitive protein detection via covalently linked aptamer to MoS and exonuclease-assisted amplification strategy.

Molybdenum disulfide (MoS) has shown highly attractive superiority as a platform for sensing. However, DNA physisorption on the surface of MoS was susceptible to nonspecific probe displacement and false-positive signals. To solve these problems, we have developed a novel MoS-aptamer nanosheet biosensor for detecting thrombin using a covalently linked aptamer to the MoS nanosheet.

Protein determination using graphene oxide-aptamer modified gold nanoparticles in combination with Tween 80.

Recently, graphene oxide (GO) has shown superiority for disease detection arising from its unique physical and chemical properties. However, proteins adsorbed on the surface of GO prevent sensitivity improvement in fluorescence-based detection methods. In this paper, a label-free method based on aptamer modified gold nanoparticles (GNPs) combined with Tween 80 was shown to solve this problem using the detection of thrombin as an example.