Open AccessMetformin directly suppresses atherosclerosis in normoglycaemic mice via haematopoietic adenosine monophosphate-activated protein kinase
Author(s) -
Anusha N. Seneviratne,
Luke Cave,
Gareth Hyde,
Søren K. Moestrup,
David Carling,
Justin C. Mason,
Dorian O. Haskard,
Joseph J. Boyle
Publication year - 2020
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvaa171
Subject(s) - metformin , ampk , medicine , endocrinology , gene knockdown , haematopoiesis , cancer research , protein kinase a , biology , microbiology and biotechnology , diabetes mellitus , kinase , apoptosis , stem cell , biochemistry
Atherosclerotic vascular disease has an inflammatory pathogenesis. Heme from intraplaque haemorrhage may drive a protective and pro-resolving macrophage M2-like phenotype, Mhem, via AMPK and activating transcription factor 1 (ATF1). The antidiabetic drug metformin may also activate AMPK-dependent signalling. Hypothesis: Metformin systematically induces atheroprotective genes in macrophages via AMPK and ATF1, thereby suppresses atherogenesis.