Abstract
We appreciate the interest in our recent study of the in vivo signalling actions of electrophilic fatty acid nitroalkenes,1 including the commentary from Tsikas et al. This study is based on a high-fat diet (HFD)-induced obesity murine model that displays the canonical features of metabolic syndrome, including glucose tolerance, vascular dysfunction, increased inflammation, adipokine dysfunction, and most notably development of pulmonary hypertension. We tested the pharmacological actions of synthetic 10-nitro-octadec-9-enoic acid (OA-NO2) and reported potent protective actions of OA-NO2 in this murine model of HFD-induced obesity and pulmonary hypertension. First and foremost, we stress that under no circumstance did we state or imply the existence of any link between obesity and decreased OA-NO2 biosynthesis. This is an incorrect and misleading interpretation of the data presented in our manuscript. The …
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