Affiliation:
1. Diabetes and Obesity Center, Department of Medicine, University of Louisville, Louisville, Kentucky
2. Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, Tennessee
3. Heart and Vascular Center, Semmelweis University, Budapest, Hungary
Abstract
Changes in CoA homeostasis have been implicated in a variety of metabolic diseases; however, the extent to which changes in CoA homeostasis impacts remodeling has not been explored. We show that limiting cardiac CoA levels via PANK deletion exacerbated ventricular remodeling during pressure overload. Our results suggest that metabolic alterations, rather than structural alterations, associated with Pank1 deletion may underlie the exacerbated cardiac phenotype during pressure overload.
Funder
Ministry of Innovation and Technology, Hungary
National Research, Development and Innovation Fund of Hungary
National Research, Development and Innovation Office (NKFIH) of Hungary
American Heart Association
HHS | NIH | NIH Office of the Director
HHS | NIH | National Heart, Lung, and Blood Institute
HHS | NIH | National Institute of General Medical Sciences
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Cited by
10 articles.
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