Association between short-term exposure to ambient air pollution and heart failure: An updated systematic review and meta-analysis of more than 7 million participants.

Introduction: Exposure to air pollution has been linked to the mortality of heart failure. In this study, we sought to update the existing systematic review and meta-analysis, published in 2013, to further assess the association between air pollution and acute decompensated heart failure, including hospitalization and heart failure mortality. Methods: PubMed, Web of Science, EMBASE, and OVID databases were systematically searched till April 2022. We enrolled the studies regarding air pollution exposure and heart failure and extracted the original data to combine and obtain an overall risk estimate for each pollutant. Results: We analyzed 51 studies and 7,555,442 patients. Our results indicated that heart failure hospitalization or death was associated with increases in carbon monoxide (3.46% per 1 part per million; 95% CI 1.0233-1.046, P < 0.001), sulfur dioxide (2.20% per 10 parts per billion; 95% CI 1.0106-1.0335, P < 0.001), nitrogen dioxide (2.07% per 10 parts per billion; 95% CI 1.0106-1.0335, P < 0.001), and ozone (0.95% per 10 parts per billion; 95% CI 1.0024-1.0166, P < 0.001) concentrations. Increases in particulate matter concentration were related to heart failure hospitalization or death (PM2.5 1.29% per 10 µg/m3, 95% CI 1.0093-1.0165, P < 0.001; PM10 1.30% per 10 µg/m3, 95% CI 1.0102-1.0157, P < 0.001). Conclusion: The increase in the concentration of all pollutants, including gases (carbon monoxide, sulfur dioxide, nitrogen dioxide, ozone) and particulate matter [(PM2.5), (PM10)], is positively correlated with hospitalization rates and mortality of heart failure. Systematic review registration: https://www.crd.york.ac.uk/PROSPERO/, identifier: CRD42021256241.

Adenovirus-mediated prothymosin α gene transfer inhibits the development of atherosclerosis in ApoE-deficient mice.

Prothymosin α (ProT) is involved in regulating expression of the oxidative stress-protective genes and it also exerts immunomodulatory activities. In this study, we investigated the therapeutic effects of ProT gene transfer on atherosclerosis in endothelial cells and in ApoE-deficient mice. Adenoviruses encoding mouse ProT (AdProT) were used for the management of atherosclerosis. In vitro, the effects of ProT on antioxidant gene expressions and the protection effect against oxidant-mediated injury in endothelial cells were examined. In vivo, AdProT were administered intraventricularly into the heart of ApoE(-/-) mice. Histopathological and immunohistochemical assessments of the aortic tissues were performed. Expressions of HO-1 and antioxidant genes in the aortic tissues were also determined. Our results demonstrated that ProT gene transfer increased antioxidant gene expressions, eNOS expression and NO release, as well as reduced the reactive oxygen species production in endothelial cells. Intraventricular administration of AdProT reduced the lesion formation, increased expressions of HO-1 and SOD genes, and reduced infiltrating macrophages in the aorta of ApoE(-/-) mice. This study suggests that ProT gene transfer may have the therapeutic potential for the management of atherosclerosis via inducing antioxidant gene expressions, eNOS expression and NO release, reducing ROS production and macrophage infiltration in endothelium.