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Thus, 15LO1 pathwayinduced redox biology perturbations worsen T2 inflammation and asthma control, supporting 15LO1 as a therapeutic target
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28 , gaab071 (2022)
Many cardiovascular risk factors such as diabetes mellitus, hypertension and hyperlipidemia are demonstrated to stimulate the interaction of Cav-1 and eNOS, reduce nitric oxide production resulting in endothelial dysfunction and subsequently the formation of atherosclerotic lesion 41,42,43
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