Diabetes propels the risk for cardiovascular disease: sweet monocytes becoming aggressive? View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-12

AUTHORS

Janna A. van Diepen, Kathrin Thiem, Rinke Stienstra, Niels P. Riksen, Cees J. Tack, Mihai G. Netea

ABSTRACT

Diabetes strongly predisposes to cardiovascular disease (CVD), the leading cause of mortality in these patients, as well as in the entire population. Hyperglycemia is an important cardiovascular risk factor as shown by the observation that even transient periods of hyperglycemia, despite return to normoglycemia during follow-up, increase the risk for CVD, a phenomenon termed 'hyperglycemic memory'. The molecular mechanisms underlying this phenomenon remain largely unknown. As inflammation plays an important role in the pathogenesis of atherosclerosis, we propose that long-term functional reprogramming of monocytes and macrophages, induced by hyperglycemia, plays an important role in the phenomenon of hyperglycemic memory leading to cardiovascular complications in patients with diabetes. In this review, we discuss recent insights showing that innate immune cells possess the capacity to reprogram their function through epigenetically mediated rewiring of gene transcription, a process termed 'trained immunity'. The long-term reprogramming of monocytes can be induced by microbial as well as metabolic products, and involves a shift in cellular metabolism from oxidative phosphorylation to aerobic glycolysis. We hypothesize that hyperglycemia in diabetes patients induces long-term activation of monocytes and macrophages through similar mechanisms, thereby contributing to plaque development and subsequent macrovascular complications. More... »

PAGES

4675-4684

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00018-016-2316-9

DOI

http://dx.doi.org/10.1007/s00018-016-2316-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010646456

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27469259


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