Acute kidney injury (AKI) is a clinical syndrome that results from a rapid decline in renal structure or renal functional impairment with the main pathological feature of sublethal and lethal damage to renal tubular cells. However, many potential therapeutic agents cannot achieve the desired therapeutic effect because of their poor pharmacokinetics and short retention time in the kidneys. With the recent emergence and progress of nanotechnology, nanodrugs with unique physicochemical properties could prolong circulation time, enhance efficient targeted delivery, and elevate the accumulation of therapeutics that can cross the glomerular filtration barrier and indicate comprehensive application prospects in the prevention and treatment of AKI. In this review, various types of nanosystems (such as liposomes, polymeric nanosystems, inorganic nanoparticles and cell-derived extracellular vesicles) are designed and applied to improve the pharmacokinetics of drug formation, which could further relieve the burden on the kidneys caused by the final cumulative dose of drugs in conventional treatments. Moreover, the passive or active targeting effect of nanosystems can also reduce the total therapeutic dose and off-target adverse effects on other organs. Nanodelivery systems for treating AKI that alleviate oxidative stress-induced renal cell damage and regulate the inflammatory kidney microenvironment are summarized.

The aim of this study was to investigate the potential association between retinol intake and the risk of chronic kidney disease (CKD) in individuals with type 2 diabetes mellitus (T2DM). The study included individuals diagnosed with T2DM between 2009 and 2018 from the NHANES database. Demographic and laboratory test data were collected for these individuals, as well as information on CKD diagnosis. Logistic regression models were utilized to estimate the relationship between different retinol intakes and the risk of CKD in patients with T2DM. A total of 3988 patients were included in the study. The mean prevalence of CKD in the T2DM population in the United States from 2009 to 2018 was 36.98 (0.02)%. Multivariate logistic regression analysis revealed a 26% decrease in the incidence of CKD in individuals with higher retinol intake compared to those with lower retinol intake in T2DM (OR = 0.74; 95% CI 0.56–0.98). Furthermore, an increase in retinol intake per 1-standard deviation (SD) was associated with a 16% decreased risk of the incidence of CKD (OR = 0.84; 95% CI 0.72–0.97). Lower retinol intake is an independent risk factor for the onset of CKD in patients with T2DM, and augmenting moderate quantities of retinol confers potential nephroprotective advantages.

Nanodelivery systems combining photothermal therapy (PTT) and chemotherapy (CT), have been widely used to improve the efficacy and biosafety of chemotherapeutic agents in cancer. In this work, we constructed a self-assembled nanodelivery system, formed by the assembling of photosensitizer (IR820), rapamycin (RAPA), and curcumin (CUR) into IR820-RAPA/CUR NPs, to realize photothermal therapy and chemotherapy for breast cancer. The IR820-RAPA/CUR NPs displayed a regular sphere, with a narrow particle size distribution, a high drug loading capacity, and good stability and pH response. Compared with free RAPA or free CUR, the nanoparticles showed a superior inhibitory effect on 4T1 cells in vitro. The IR820-RAPA/CUR NP treatment displayed an enhanced inhibitory effect on tumor growth in 4T1 tumor-bearing mice, compared to free drugs in vivo. In addition, PTT could provide mild hyperthermia (46.0 °C) for 4T1 tumor-bearing mice, and basically achieve tumor ablation, which is beneficial to improving the efficacy of chemotherapeutic drugs and avoiding damage to the surrounding normal tissue. The self-assembled nanodelivery system provides a promising strategy for coordinating photothermal therapy and chemotherapy to treat breast cancer.

Radiation nephropathy refers to kidney damage caused by radiation therapy for malignant tumours. Currently, the pathogenesis is unclear and there is a lack of effective treatment methods. With the development of traditional Chinese medicine, the role of traditional Chinese medicine in the protection of radiation nephropathy is receiving increasing attention. Therefore, in this study, we used X-ray intraperitoneal irradiation to construct a mouse model of radiation nephropathy and studied the protective effect of traditional Chinese medicine Keluoxin on radiation nephropathy. We first analysed the potential targets and pathways of Keluoxin in the treatment of radiation nephropathy using network pharmacology methods, combined with in vitro and in vivo experimental verification, to study its potential mechanism. By searching the database, 136 components of Keluoxin were identified. A total of 333 intersectional targets related to radiation nephropathy were obtained. Among them, key targets include IL-6, TNF-α, HIF-1α, STAT1, STAT3, JAK1, JAK2, etc. In in vivo and in vitro experiments, we found that as the irradiation dose increased and time prolonged, kidney damage in mice gradually worsened in a time-dependent and dose-dependent manner. As the irradiation dose increases, the expression of pro-inflammatory factors Il-6, TNF-α, TGF-β increased. Compared with the irradiation group, the intervention of Keluoxin can reduce kidney damage caused by X-ray irradiation and reduce the expression of IL-6, TNF-α, TGF-β, STAT1, STAT3, JAK1, JAK2, etc. These results indicated that Keluoxin can alleviate kidney damage caused by X-ray irradiation, possibly by regulating the JAK/STAT signalling pathway, reducing inflammation levels and oxidative stress damage.

Background: Vascular calcification (VC) is a significant risk factor for cardiovascular disease. The pathogenesis involves various factors such as hyperphosphatemia, oxidative stress, inflammation, and apoptotic cell death, leading to phenotypic changes in vascular smooth muscle cells (VSMCs) and subsequent calcification. This study aims to investigate the impact of roxadustat, a hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHI), on the development of calcification in VSMCs induced by hyperphosphatemia in mice. Methods: Aortic VSMCs were cultured and exposed to high phosphate conditions to induce calcification. The cells were divided into control, high phosphate, and HIF-PHI plus high phosphate groups. Cell viability was assessed using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay, and calcium content was measured through Von Kossa staining and the bicinchoninic acid (BCA) assay. The apoptotic rate was determined by flow cytometry, alkaline phosphatase concentration was determined by enzyme-linked immunosorbent assay (ELISA), and mitochondrial reactive oxygen species (ROS) levels were determined by Dichlorodihydrofluorescein acetoacetate (DCFH-DA). Protein expression levels were evaluated using immunoblotting techniques. Results: Compared to the control group, calcium deposition, calcium content, alkaline phosphatase, Runt-related Transcription Factor 2 (RUNX2) expression and apoptotic rate were significantly higher, while Alpha Smooth Muscle Actin (α-SMA) expression was significantly lower in the high phosphate group (p < 0.05). The HIF-PHI group showed an opposite trend to the high phosphate group in a dose-dependent manner (p < 0.05). The mitochondrial ROS and BCL2/adenovirus E1B 19kDa protein-interacting protein 3-like (BNIP3L) expression were significantly higher in the high phosphate group than in the control group (p < 0.05). Compared to the high phosphate group, the mitochondrial ROS was lower, while the protein expression levels of BNIP3L and Bcl-2 Interacting Protein 1 (Beclin-1) were higher in the HIF-PHI group (p < 0.05). HIF-1α protein expression was significantly higher in the high phosphate group than in the control group, which was increased by the treatment of HIF-PHI (p < 0.05). Conclusions: HIF-PHI ameliorates vascular calcification and apoptosis in high-phosphate induced viability of VSMCs by upregulation of HIF-1α expression, reduced mitochondrial ROS production and increased expression of autophagy-related proteins.