Background:Studies on the effect of air pollutions on kidney diseases are still limited.Objective:We aimed to investigate the associations between particulate matter (PM) exposures and renal function among adults.Methods:We recruited 21,656 adults as participants from 2007 to 2009. The Taiwanese Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation was used to derive the estimated glomerular filtration rate (eGFR). Subjects with an eGFR lower than 60 mL/min/1.73 m2 were defined as having chronic kidney disease (CKD). Land use regression (LUR) models were used to estimate individual exposures to PM with an aerodynamic diameter < 10 μm (PM10), coarse particles (PMCoarse), fine particles (PM2.5), and PM2.5Absorbance. Generalized linear and logistic regression models were used to estimate the associations between PM exposure and renal function.Results:An IQR increase in PM10 (5.83 μg/m3) was negatively associated with eGFR by –0.69 (95% CI: –0.89, –0.48) mL/min/1.73 m2 and positively associated with the prevalence of CKD with adjusted OR = 1.15 (95% CI: 1.07, 1.23). An IQR increase in PMCoarse (6.59 μg/m3) was significantly associated with lower eGFR by –1.07 (95% CI: –1.32, –0.81) mL/min/1.73 m2 and CKD with OR = 1.26 (95% CI: 1.15, 1.38). In contrast, neither outcome was significantly associated with PM2.5 or PM2.5Absorbance. Stratified analyses indicated that associations of CKD with both PM10 and PMCoarse were limited to participants < 65 years of age, and were stronger (for PM10) or limited to (PMCoarse) women. Associations also appeared to be stronger in those without (vs. with) hypertension, and in normal versus overweight participants.Conclusions:Exposure during the previous year to PM10 and PMCoarse, but not PM2.5 or PM2.5Absorbance, was associated with reduced renal function among Taiwanese adults.Citation:Yang YR, Chen YM, Chen SY, Chan CC. 2017. Associations between long-term particulate matter exposure and adult renal function in the Taipei metropolis. Environ Health Perspect 125:602–607; http://dx.doi.org/10.1289/EHP302

No abstract

Recently, circular RNAs (circRNAs) have been frequently reported to be involved in hepatocellular carcinoma (HCC) development and progression. However, the role of circRNAs in hepatic fibrosis (HF) is still unclear. Our previous highthroughput screen revealed changes in many circRNAs in mice with carbon tetrachloride (CCl 4 )-induced HF. For instance, the expression of circPSD3, a circRNA derived from the Pleckstrin and Sec7 domain-containing 3 (PSD3) gene, was considerably downregulated in primary hepatic stellate cells (HSCs) and liver tissues of mice with CCl 4 -induced HF compared to those in the vehicle group. In vivo overexpression of circPSD3 using AAV8-circPSD3 arrested the deterioration of CCl 4 -induced HF as indicated by reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) content, liver hydroxyproline level, collagen deposition, and pro-fibrogenic gene and pro-inflammatory cytokine levels. Moreover, in vitro loss-of-function and gain-of-function analyses suggested that circPSD3 inhibited the activation and proliferation of HSCs. Mechanistically, circPSD3 served as a sponge for miR-92b-3p, subsequently promoting the expression of Smad7. In conclusion, our present findings reveal a novel mechanism by which circPSD3 alleviates hepatic fibrogenesis by targeting the miR-92b-3p/Smad7 axis, and they also indicate that circPSD3 may serve as a potential biomarker for HF.

No abstract