https://www.selleckchem.com/products/AP24534.html
The presence of PM specifically enhanced oxidative stress and inflammatory reactions under subchronic exposure to traffic-related PM and suppressed glucose metabolism and actin cytoskeleton signalling. These factors might lead to repair failure and thus to lung function decline after chronic exposure to traffic-related PM . A detailed pathogenic mechanism was proposed to depict temporal and dynamic molecular regulations associated with PM - and gaseous pollutants-induced lung injury. This study explored several potential molecular featu
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