Melatonin ameliorates glyphosate- and hard water-induced renal tubular epithelial cell senescence via PINK1-Parkin-dependent mitophagy.

The combination of glyphosate (Gly) and hard water (Hwt) is a suspected risk factor for chronic interstitial nephritis in agricultural communities (CINAC). Accumulated mitochondrial damage and proximal tubular epithelial (PTE) cell senescence have been implicated in CINAC pathogenesis. Melatonin (Mel) has potential mitochondrial function and renoprotective properties, but its role and mechanism in CINAC are unknown.

Melatonin ameliorates renal dysfunction in glyphosate- and hard water-treated mice.

Chronic interstitial nephritis in agricultural communities (CINAC) is a severe and widespread disease that has been associated with environmental and occupational exposure to glyphosate and hard water. However, the potential underlying mechanisms remain incompletely understood. Melatonin is reported to exert protective effects on the kidney, but whether melatonin can attenuate renal tubular injury in mice exposed to glyphosate combined with hard water is unclear.

Construction and validation of a novel ten miRNA-pair based signature for the prognosis of clear cell renal cell carcinoma.

Background: Clear cell renal cell carcinoma (ccRCC) is the most predominate pathological subtype of renal cell carcinoma, causing a recurrence or metastasis rate as high as 20% to 40% after operation, for which effective prognostic signature is urgently needed.

Methods: The mRNA and miRNA profiles of ccRCC specimens were collected from the Cancer Genome Atlas. MiRNA-pair risk score (miPRS) for each miRNA pair was generated as a signature and validated by univariate and multivariate Cox proportional hazards regression analysis.

Short sleep duration increases the risk of hyperuricemia among Chinese adults: findings from the China Health and Nutrition Survey.

Study Objectives: Hyperuricemia is a growing public health problem with its increasing prevalence. Few studies have investigated the association between sleep duration and hyperuricemia. The objective of this study is to explore whether short sleep duration is an independent risk factor of hyperuricemia in Chinese adults.

Association between exposure to the Chinese famine during early life and the risk of chronic kidney disease in adulthood.

Background And Objectives: Famine exposure in human early life is proven to be associated with urinary protein concentration and renal function but has not been studied with chronic kidney disease. We aimed to explore the association between exposure to the Chinese famine (from 1959 to 1962) in early life and the risk of chronic kidney disease in adulthood.

Design, Setting, Participants, And Measurements: We selected 6267 participants from the baseline survey of China Health and Retirement Longitudinal Study (CHARLS) 2011-2012.

METTL14-dependent m6A regulates vascular calcification induced by indoxyl sulfate.

Aims: Although the functional importance of N6-methyladenosine (m6A) in various fundamental bioprocesses are well known, its effect on vascular calcification is not well studied. We investigated the role of methyltransferase-like 14 (METTL14), an m6A methylase, in vascular calcification.

Main Methods: We used clinical human samples as well as rat models and primary human artery smooth muscle cell (HASMC) cultures to study the functional role of m6A and METTL14 in vascular calcification and in HASMCs.

Association of urinary ionomic profiles and acute kidney injury and mortality in patients after cardiac surgery.

Objective: The rarity of sensitive biomarkers for acute kidney injury (AKI) has impeded the timely therapy of AKI. Emerging evidence suggests that ion homeostasis may play pertinent roles in AKI. We aimed to screen out representative urinary ions and build a cardiac surgery-associated AKI indication model.

Gap junctional intercellular communication and endoplasmic reticulum stress regulate chronic cadmium exposure induced apoptosis in HK-2 cells.

Cadmium (Cd), a toxic heavy metal, is known to induce renal toxicity by primarily targeting at renal proximal tubule. Endoplasmic reticulum (ER) stress and gap junctional intercellular communication (GJIC) regulate many pathophysiological processes. Yet, how ER stress and GJIC regulate Cd-induced nephrotoxicity remain elusive.

Indoxyl sulfate accelerates vascular smooth muscle cell calcification via microRNA-29b dependent regulation of Wnt/β-catenin signaling.

Vascular calcification (VC) is a very common phenomenon in patients with chronic kidney disease(CKD) and it increases the incidence of cardiovascular disease and leads to high mortality in CKD patients. It has been reported that some microRNAs (miRs) play roles in vascular calcification as an epigenetic regulator. Indoxyl sulfate (IS) is a protein-bound uremic toxin which has been proven as one of the major risk factors of cardiovascular disease in CKD.