Short or long sleep duration was associated with chronic kidney disease in a Chinese nationwide cohort study.

OBJECTIVE: Sleep duration is an important factor influencing health outcomes. The association between sleep duration and kidney function remains elusive. This study aimed to explore the association between sleep duration and chronic kidney disease (CKD) amongst Chinese adults. METHODS: We conducted a cross-sectional study based on the China Health and Nutrition Survey (CHNS) in the wave of 2009. Participants were divided into three groups: ≤ 6 h/day (short sleepers), 7-8 h/day (regular sleepers) and ≥ 9 h/day (long sleepers) according to self-reported sleep duration. CKD was defined as estimated glomerular filtration rate < 60 mL/min/1.73 m2. RESULTS: A total of 8096 Chinese adults (45.9% men) with a mean age of 50.6 years were included in the study. Compared with regular sleepers, both short and long regular sleepers had a higher prevalence of CKD. A U-shaped relationship between sleep duration and CKD was displayed by restricted cubic spline curve (P-overall < 0.001, P-nonlinear < 0.001). Multivariate logistic regression models revealed that both short and long sleep duration were clinically associated with higher odds of CKD, after adjustments for covariates [adjusted odds ratio (OR) 1.25 and 1.30; 95% confidence interval (CI) 1.00-1.56 and 1.08-1.54, for short and long sleep duration, respectively]. In subgroup analyses, we found the association was still observed in participants without hypertension or diabetes mellitus. CONCLUSION: Short or long sleep duration was associated with CKD in the general population.

Eupatilin inhibits pulmonary fibrosis by activating Sestrin2/PI3K/Akt/mTOR dependent autophagy pathway.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive chronic inflammatory disease with poor clinical outcomes and ineffective drug treatment options. Eupatilin is a major component extracted from the traditional herbal medicine Artemisia asiatica Nakai. Notably, it was demonstrated to have an anti-fibrosis effect in endometrial fibrosis, vocal fold, and hepatic fibrosis. Its role and mechanism in IPF remain unclear. METHODS: This study used the TGF-ß1-induced human embryonic lung fibroblasts (MRC-5) activation, IPF lung fibroblasts, and bleomycin-induced lung fibrosis mice model. Western blot, immunofluorescence staining, quantitative real time-PCR, hematoxylin and eosin staining, Masson's trichrome staining, and immunohistochemistry were used to evaluate the effects of eupatilin on fibroblast activation, pulmonary fibrosis, and autophagy. The autophagosomes were observed with a transmission electron microscope (TEM). RNA sequencing was used to determine the signaling pathway and key regulator related to autophagy. RESULTS: Eupatilin significantly decreased the expression of Col1A1, fibronectin, α-SMA, and SQSTM1/p62. In contrast, it increased the expression of LC3B II/I and the number of autophagosomes in TGF-ß1 treated MRC-5, IPF lung fibroblasts, and bleomycin-induced lung fibrosis mice model; it also alleviated bleomycin-induced lung fibrosis. The KEGG pathway mapping displayed that PI3K/Akt and Sestrin2 were associated with the enhanced fibrogenic process. Eupatilin suppressed the phosphorylation of PI3K/Akt/mTOR. Autophagy inhibitor 3-methyladenine (3-MA) and Akt activator SC-79 abrogated the anti-fibrotic effect of eupatilin. Sestrin2 expression was also downregulated in TGF-ß1 treated lung fibroblasts and lung tissues of the bleomycin-induced pulmonary fibrosis mice model. Furthermore, eupatilin promoted Sestrin2 expression, and the knockdown of Sestrin2 significantly aggravated the degree of fibrosis, increased the phosphorylation of PI3K/Akt/mTOR, and decreased autophagy. CONCLUSION: These findings indicate that eupatilin ameliorates pulmonary fibrosis through Sestrin2/PI3K/Akt/mTOR-dependent autophagy pathway.

Non-coding RNAs: Important participants in cardiac fibrosis.

Cardiac remodeling is a pathophysiological process activated by diverse cardiac stress, which impairs cardiac function and leads to adverse clinical outcome. This remodeling partly attributes to cardiac fibrosis, which is a result of differentiation of cardiac fibroblasts to myofibroblasts and the production of excessive extracellular matrix within the myocardium. Non-coding RNAs mainly include microRNAs and long non-coding RNAs. These non-coding RNAs have been proved to have a profound impact on biological behaviors of various cardiac cell types and play a pivotal role in the development of cardiac fibrosis. This review aims to summarize the role of microRNAs and long non-coding RNAs in cardiac fibrosis associated with pressure overload, ischemia, diabetes mellitus, aging, atrial fibrillation and heart transplantation, meanwhile shed light on the diagnostic and therapeutic potential of non-coding RNAs for cardiac fibrosis.