Targeting WNT5A noncanonical signaling attenuates renal fibrosis progression in acute kidney injury.

Preventing the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remains a considerable clinical challenge. In this study, we elucidate the role of WNT5A in accelerating the AKI-to-CKD transition and its underlying mechanisms. Renal biopsies from patients with AKI showed marked upregulation of WNT5A and its receptor, CD146, in proximal tubules, with higher expression in patients with CKD progression.

Controllable Cyclic Wet Etching of Molybdenum at Room Temperature.

A cyclic wet etching process for molybdenum (Mo) film utilizing ammonium persulfate (APS) solution at room temperature has been developed, enabling precise etching of the Mo film. The etch per cycle (EPC) of the Mo film was determined to be 0.3 nm/cycle in the 1 wt % APS solution.

Association Between Urinary Metals and Polycyclic Aromatic Hydrocarbon Levels and Cardiovascular Disease Among Adult Americans: Data from NHANES 2011 to 2016.

Previous studies have inconclusively examined the associations of metals or polycyclic aromatic hydrocarbons (PAHs) with cardiovascular disease (CVD) separately, highlighting the need to explore their combined association with CVD. Based on the 2011-2016 National Health and Nutrition Examination Survey, the association of 12 metals and six PAHs in urine with CVD was analyzed using weighted logistic regression, weighted quantile sum (WQS) regression, and Bayesian kernel machine regression (BKMR). Crucial metals and PAHs were screened, and dose-response, subgroup, interactions, and mediation analyses were conducted.

The Noncanonical Wnt5a-Ca Pathway Mediates Mitochondrial Dysfunction in the Progression of Diabetic Nephropathy via the Mitochondrial Calcium Uniporter.

Abnormal Wnt5a expression, mitochondrial abnormalities and calcium overload have been detected in many metabolic diseases. However, the association of Wnt5a-Ca and mitochondrial dysfunction in diabetic nephropathy (DN) progression remains unknown. We used streptozotocin-induced DBA2/J male mice as a DN model.

Serum sodium to chloride ratio and mortality on continuous ambulatory peritoneal dialysis: a multicenter retrospective study.

An imbalance in the serum sodium to chloride ratio (Na/Cl) was linked to higher mortality among heart failure patients. Nonetheless, the prognostic significance of Na/Cl in individuals undergoing peritoneal dialysis (PD) remains unexplored. This study seeks to explore the association between initial Na/Cl levels and mortality in PD patients.

Histone lactylation-driven YTHDC1 promotes hepatocellular carcinoma progression via lipid metabolism remodeling.

Lipid metabolism reprogramming is critical for the initiation and progression of hepatocellular carcinoma (HCC). However, how the dysregulation of lipid metabolism contributes to HCC development remains largely unknown. Here, we report that the mA reader YTHDC1-mediated epigenetic regulation of the long noncoding RNA NEAT1 activates stearoyl-CoA desaturase (SCD)-associated lipid metabolic processes during HCC progression.

Incorporation of Chest Computed Tomography Quantification to Predict Outcomes for Patients on Hemodialysis with COVID-19.

Introduction: Patients undergoing maintenance hemodialysis are vulnerable to coronavirus disease 2019 (COVID-19), exhibiting a high risk of hospitalization and mortality. Thus, early identification and intervention are important to prevent disease progression in these patients.

Methods: This was a two-center retrospective observational study of patients on hemodialysis diagnosed with COVID-19 at the Lingang and Xuhui campuses of Shanghai Sixth People's Hospital.

Screening and evaluation of antioxidants for retinal pigment epithelial cell protection: L-ergothioneine as a novel therapeutic candidate through NRF2 activation.

The continual exposure of retinal tissues to oxidative stress leads to discernible anatomical and physiological alterations. Specifically, the onslaught of oxidative damage escalates the irreversible death of retinal pigmented epithelium (RPE) cells, pinpointed as the fundamental pathological event in dry age-related macular degeneration (AMD). There is a conspicuous lack of effective therapeutic strategies to counteract this degenerative process.

Cardiac-specific renalase overexpression alleviates CKD-induced pathological cardiac remodeling in mice.

Introduction: CKD-induced pathological cardiac remodeling is characterized by myocardial hypertrophy and cardiac fibrosis. The available therapeutic options are limited, it is thus urgently needed to identify novel therapeutic targets. Renalase (RNLS) is a newly discovered protein secreted by the kidney and was found beneficial in many renal diseases.

Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis.

Forkhead box C1 (FOXC1) is required for neural crest and ocular development, and mutations in FOXC1 lead to inherited Axenfeld-Rieger syndrome. Here, we find that FOXC1 and paired box 6 (PAX6) are co-expressed in the human limbus and central corneal epithelium. Deficiency of FOXC1 and alternation in epithelial features occur in patients with corneal ulcers.

D609 protects retinal pigmented epithelium as a potential therapy for age-related macular degeneration.

Accumulated oxidative damage may lead to irreversible retinal pigmented epithelium (RPE) cell death, which is considered to be the primary cause of dry age-related macular degeneration (AMD), leading to blindness in the elderly. However, an effective therapy for this disease is lacking. Here, we described a robust high-content screening procedure with a library of 814 protective compounds and found that D609 strongly protected RPE cells from sodium iodate (SI)-induced oxidative cell death and prolonged their healthy survival.

UBE3A alleviates isoproterenol-induced cardiac hypertrophy through the inhibition of the TLR4/MMP-9 signaling pathway.

Cardiac hypertrophy is considered to be a leading factor in heart function-related deaths. In this study, we explored the potential mechanism underlying cardiac hypertrophy induced by isoproterenol. Our results showed that isoproterenol induced cardiac hypertrophy in AC16 cells, as reflected by the increased cell surface area and increased hypertrophic markers, which was accompanied by increased ubiquitin-protein ligase E3a (UBE3A) expression.