Comment on “Pharmacological inhibition of protein tyrosine phosphatase 1B protects against atherosclerotic plaque formation in the LDLR-/- mouse model of atherosclerosis”.

[Extract] We read with great interest the recent article by Thompson and colleagues [1] which reported the effects of inhibiting protein tyrosine phosphatase 1B (PTP1B) on the development of atherosclerosis within low-density lipoprotein receptor deficient (LDLR−/−) mice receiving either chow or high-fat diet. In this study, the authors conducted two experiments in which mice received single or five doses of the specificPTP1B inhibitor, trodusquemine. In both experiments, the investigators reported that when compared with controls, mice receiving trodusquemine exhibited a significant decrease in weight gain paralleled by marked improvements in glycaemic control and lipid profile. A key finding was the observation of a significantly lower atherosclerotic plaque area within the aortic root in high fat fed mice which received trodusequemine, compared with the saline controls. This led the authors to conclude that inhibition of PTP1B‘...resulted in both the reduction and reversal of atherosclerotic plaque formation under obesogenic conditions.’ Identification of drugs with the ability to reverse the severity of established atherosclerosis has a significant potential to improve patient care. The findings of this study are therefore of great interest to the field and have led to substantial media attention. We believe, however, that the authors’ statements are misleading