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Publication
Regulating MicroRNA Expression: At the Heart of Diabetes Mellitus and the
Mitochondrion.
Authors
Hathaway QA, Pinti MV, Durr AJ, Waris S, Shepherd DL, Hollander JM
Submitted By
John Hollander on 11/8/2017
Status
Published
Journal
American journal of physiology. Heart and circulatory physiology
Year
2017
Date Published
10/1/2017
Volume : Pages
Not Specified
: ajpheart.0
PubMed Reference
28986361
Abstract
Type 2 diabetes mellitus is a major risk factor for cardiovascular disease and
mortality. Uncontrolled type 2 diabetes mellitus results in a systemic milieu of
increased circulating glucose and fatty acids. The development of insulin
resistance in cardiac tissue decreases cellular glucose import and enhances
mitochondrial fatty acid uptake. While triacylglycerol and cytotoxic lipid
species begin to accumulate in the cardiomyocyte, the energy substrate
utilization ratio of free fatty acids (FFAs) to glucose changes to almost
entirely FFAs. Accumulating evidence suggests a role of microRNA (miRNA) in
mediating this metabolic transition. Energy substrate metabolism, apoptosis, and
the production and response to excess reactive oxygen species (ROS) are
regulated by miRNA expression. The current momentum for understanding the
dynamics of miRNA expression is limited by a lack of understanding how miRNA
expression is controlled. While miRNAs are important regulators in both normal
and pathological states, an additional layer of complexity is added when
regulation of the miRNA regulators is considered. MiRNA expression is known to
be regulated through a number of mechanisms which include, but are not limited
to, epigenetics, exosomal transport, processing, and post-transcriptional
sequestration. The purpose of this review is to outline how mitochondrial
processes are regulated by miRNAs in the diabetic heart. Further, we will
highlight the regulatory mechanisms such as epigenetics, exosomal transport,
miRNA processing, and post-translational sequestration that participate as
regulators of miRNA expression. Additionally, current and future treatment
strategies targeting dysfunctional mitochondrial processes in diseased
myocardium as well as emerging miRNA-based therapies will be summarized.
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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