Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed-forward loop between LXR and autophagy

Journal of Internal Medicine

1 Luglio Lug 2019 one month ago
  • Baldassarre D, Tremoli E, Veglia F

Hyperlipidemia is a major risk factor for cardiovascular disease and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts.

Reference

Saliba-Gustafsson P, Pedrelli M, Gertow K, Werngren O, Janas V, Pourteymour S, Baldassarre D, Tremoli E, Veglia F, Rauramaa R, Smit AJ, Giral P, Kurl S, Pirro M, de Faire U, Humphries SE, Hamsten A; IMPROVE study group, Gonçalves I, Orho-Melander M, Franco-Cereceda A, Borén J, Eriksson P, Magné J, Parini P, Ehrenborg E. Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed-forward loop between LXR and autophagy. J Intern Med 2019 Jun 28. doi: 10.1111/joim.12951.

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