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This corrects the article: “Ioannou A. Evolution of Disease-modifying Therapy for Transthyretin Cardiac Amyloidosis. Heart International. 2024;18(1):30-37”. Two typography errors were included incorrectly due to an editorial error. In Table 1, “eplontersen” was incorrectly written as “eplomtersen”. This has been corrected in the text. In the section “Eplontersen”, the administration schedule should be written as […]

Role of the IRS-1 and/or -2 in the pathogenesis of insulin resistance in Dahl salt-sensitive (S) rats

Marlene F. Shehata
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Published Online: Jul 30th 2018 Heart International 2009;4(1):e6 DOI: https://doi.org/10.4081/hi.2009.e6
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Abstract

Overview

Insulin resistance is a common finding in
hypertensive humans and animal models. The
Dahl salt-sensitive (S) rat is an ideal model of
genetically predetermined insulin resistance
and salt-sensitive hypertension. Along the
insulin signaling pathway, the insulin receptor
substrates 1 and 2 (IRS-1 and -2) are important
mediators of insulin signaling. IRS-1
and/or IRS-2 genetic variant(s) and/or
enhanced serine phosphorylation correlate
with insulin resistance. The present commentary
was designed to highlight the significance
of IRS-1 and/or -2 in the pathogenesis of
insulin resistance. An emphasis will be given
to the putative role of IRS-1 and/or -2 genetic
variant(s) and serine phosphorylation in precipitating
insulin resistance.

Keywords

Dahl S rats, insulin resistance, saltsensitivity, insulin signaling pathway, genetic contributors, molecular contributors.

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Article Information

Correspondence

Marlene Shehata, 207-1140 Fisher Avenue, K1Z 8M5, Ottawa, ON, Canada. E-mail: marlenefouad@yahoo.com

Received

2009-05-12T00:00:00

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