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Urocortin 2 Gene Transfer Improves Heart Function in Aged Mice.

Dimosthenis Giamouridis¹, Mei Hua Gao², N Chin Lai²

¹Department of Medicine, University of California, San Diego, Veterans Affairs San Diego Healthcare System, San Diego, CA 92161, USA; Department of Medicine, University of California San Diego, San Diego, CA, USA; Department of Pharmacology and Toxicology, Cardiovascular Research Institute Maastricht, Maastricht University, the Netherlands; Department of Pathology, Cardiovascular Research Institute, Maastricht University, the Netherlands.

Molecular Therapy : the Journal of the American Society of Gene Therapy

|November 3, 2019

Summary

Urocortin 2 (Ucn2) gene transfer improved heart function in aged mice and prevented age-related cardiac dysfunction. This therapy enhanced ejection fraction and reduced cardiac stress, offering a potential treatment for aging hearts.

Keywords:

AAV HFpEF LV strain age-related LV dysfunction contractile function diastolic function gene transfer urocortin 2

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Area of Science:

Cardiovascular Biology
Gene Therapy
Aging Research

Background:

Left ventricular (LV) systolic and diastolic dysfunction are common with aging.
Previous studies showed urocortin 2 (Ucn2) gene transfer improves heart function in heart failure with reduced ejection fraction.

Purpose of the Study:

To investigate if Ucn2 gene transfer can improve LV function in aged mice.
To determine if early-life Ucn2 gene transfer can prevent age-related LV dysfunction.

Main Methods:

Nineteen-month-old mice received Ucn2 gene transfer or saline (treatment study).
Three-month-old mice received Ucn2 gene transfer or saline (prevention study).
LV function was assessed 3-20 months post-injection, along with molecular markers of cardiac function and stress.

Main Results:

Ucn2 gene transfer increased ejection fraction, reduced LV volume, and improved contractility (peak -dP/dt and peak +dP/dt) in both treatment and prevention groups.
Ucn2 gene transfer reduced global longitudinal strain, indicating improved cardiac mechanics.
Molecularly, Ucn2 gene transfer increased SERCA2a protein, decreased CaMKIIa phosphorylation, and reduced α-skeletal actin mRNA, suggesting reduced cardiac stress.

Conclusions:

Ucn2 gene transfer effectively restores normal cardiac function in aged mice with existing LV dysfunction.
Ucn2 gene transfer administered early in life can prevent the development of age-related LV dysfunction.
Ucn2 gene therapy presents a promising strategy for combating age-related cardiac decline.