Soranno, Danielle E.Kirkbride-Romeo, LaraWennersten, Sara A.Ding, KathyCavasin, Maria A.Baker, PeterAltmann, ChristopherBagchi, Rushita A.Haefner, Korey R.Steinkühler, ChristianMontford, John R.Keith, BrysenGist, Katja M.McKinsey, Timothy A.Faubel, Sarah2022-07-262022-07-262021-02-22Soranno DE, Kirkbride-Romeo L, Wennersten SA, et al. Acute Kidney Injury Results in Long-Term Diastolic Dysfunction That Is Prevented by Histone Deacetylase Inhibition. JACC Basic Transl Sci. 2021;6(2):119-133. Published 2021 Feb 22. doi:10.1016/j.jacbts.2020.11.013https://hdl.handle.net/1805/29652Growing 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.en-USAttribution-NonCommercial-NoDerivatives 4.0 InternationalAcute kidney injuryCardiorenal syndromeDiastolic dysfunctionHistone deacetylase inhibitionSystemic sequelae of kidney diseaseArticle