Acute Kidney Injury Results in Long-Term Diastolic Dysfunction That Is Prevented by Histone Deacetylase Inhibition.

Abstract

Growing epidemiological data demonstrate that acute kidney injury (AKI) is associated with long-term cardiovascular morbidity and mortality. Here, the authors present a 1-year study of cardiorenal outcomes following bilateral ischemia-reperfusion injury in male mice. These data suggest that AKI causes long-term dysfunction in the cardiac metabolome, which is associated with diastolic dysfunction and hypertension. Mice treated with the histone deacetylase inhibitor, ITF2357, had preservation of cardiac function and remained normotensive throughout the study. ITF2357 did not protect against the development of kidney fibrosis after AKI.

• Authors: Danielle E Soranno, Lara Kirkbride-Romeo, Sara A Wennersten, Kathy Ding, Maria A Cavasin, Peter Baker, Christopher Altmann, Rushita A Bagchi, Korey R Haefner, Christian Steinkühler, John R Montford, Brysen Keith, Katja M Gist, Timothy A McKinsey, Sarah Faubel
• Journal: JACC. Basic to translational science (JACC Basic Transl Sci) Vol. 6 Issue 2 Pg. 119-133 (Feb 2021) ISSN: 2452-302X [Electronic] United States
• PMID: 33665513 (Publication Type: Journal Article)
• Copyright: © 2021 The Authors.