Journal
NON-CODING RNA
Volume 7, Issue 3, Pages -Publisher
MDPI
DOI: 10.3390/ncrna7030039
Keywords
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Funding
- National Institutes of Health (NIH) [R01-DK123259, R01-HL146691, R01-DK033823, R01-HL159062, R56-AG066431, T32-HL144456, R00D-K107895]
- Irma T. Hirschl and Monique Weill-Caulier Trusts
- American Heart Association [AHA-21POST836407, AHA-20POST35211151]
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Substantial evidence suggests that miR-155 plays a crucial role in the pathogenesis of diabetes mellitus and its complications, with clinical studies reporting low levels in T2D patients. It contributes to cellular changes and insulin sensitivity regulation, and dysregulation of miR-155 expression is associated with the development of diabetic complications.
Substantial evidence indicates that microRNA-155 (miR-155) plays a crucial role in the pathogenesis of diabetes mellitus (DM) and its complications. A number of clinical studies reported low serum levels of miR-155 in patients with type 2 diabetes (T2D). Preclinical studies revealed that miR-155 partakes in the phenotypic switch of cells within the islets of Langerhans under metabolic stress. Moreover, miR-155 was shown to regulate insulin sensitivity in liver, adipose tissue, and skeletal muscle. Dysregulation of miR-155 expression was also shown to predict the development of nephropathy, neuropathy, and retinopathy in DM. Here, we systematically describe the reports investigating the role of miR-155 in DM and its complications. We also discuss the recent results from in vivo and in vitro models of type 1 diabetes (T1D) and T2D, discussing the differences between clinical and preclinical studies and shedding light on the molecular pathways mediated by miR-155 in different tissues affected by DM.
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