Overexpression of interleukin-18 aggravates cardiac fibrosis and diastolic dysfunction in fructose-fed rats.

Molecular Medicine
Shan-Shan XingWei Zhang

Abstract

Inflammation plays an important role in the pathophysiology of the metabolic syndrome (MS). We determined whether the overexpression of interleukin (IL)-18 could aggravate left ventricular (LV) remodeling and diastolic dysfunction in fructose-fed rats (FFRs). To create an animal model for MS, male Wistar rats received 10% fructose in water for 8 months. We used an adenovirus encoding rat IL-18 to overexpress IL-18 in FFRs by intravenous administration. IL-18 overexpression led to increases in collagen volume fraction and collagen deposition. LV systolic function was unaltered. But the LV end-diastolic pressure and the time constant of isovolumic relaxation (tau) were increased. Peak negative value of time derivative of LV pressure (-dp/dt) was decreased. Isovolumic relaxation time and myocardial index, as assessed by echocardiography, were increased. Overexpression of IL-18 leads to aggravated LV remodeling and dysfunction in FFRs. Attenuation of the inflammatory process may provide a novel therapeutic strategy in treating metabolic cardiomyopathy.

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Citations

Mar 30, 2012·Metabolic Syndrome and Related Disorders·Dorthe StensvoldUlrik Wisløff
Jul 5, 2012·PloS One·Miriam WittmannHeiko Mühl
May 22, 2013·Journal of Diabetes Research·Alexandre M LehnenBeatriz D'Agord Schaan
Jul 30, 2019·Journal of Cardiovascular Pharmacology·Marina SokolovaPal Aukrust
Oct 5, 2019·Journal of Cardiovascular Pharmacology·Marina SokolovaPål Aukrust
Dec 25, 2019·Oxidative Medicine and Cellular Longevity·Lin-Lin KangLing-Dong Kong
Feb 11, 2021·Saudi Journal of Kidney Diseases and Transplantation : an Official Publication of the Saudi Center for Organ Transplantation, Saudi Arabia·Ahlam BadawyYasser Gamal

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