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Cell Physiol Biochem. 2018;46(4):1683-1692. doi: 10.1159/000489244. Epub 2018 Apr 20.

UCP3 Ablation Exacerbates High-Salt Induced Cardiac Hypertrophy and Cardiac Dysfunction.

Author information

1
Department of Endocrinology, Chengdu Military General Hospital, Chengdu, China.
2
Department of Neurology, Chengdu Military General Hospital, Chengdu, China.
3
Department of Cardiovascular, Chengdu Military General Hospital, Chengdu, China.

Abstract

BACKGROUND/AIMS:

Excessive salt intake and left ventricular hypertrophy (LVH) are both critical for the development of hypertension and heart failure. The uncoupling protein 3 (UCP3) plays a cardio-protective role in early heart failure development. However, the potential role for UCP3 in salt intake and LVH is unclear.

METHODS:

UCP3-/- and C57BL/6 mice were placed on either a normal-salt (NS, 0.5%) or a high-salt (HS, 8%) diet for 24 weeks. The cardiac function, endurance capacity, energy expenditure, and mitochondrial functional capacity were measured in each group.

RESULTS:

Elevated blood pressure was only observed in HS-fed UCP3-/- mice. High salt induced cardiac hypertrophy and dysfunction were observed in both C57BL/6 and UCP3-/- mice. However, the cardiac lesions were more profound in HS-fed UCP3-/- mice. Furthermore, HS-fed UCP3-/-mice experienced more severe mitochondrial respiratory dysfunction compared with HS-fed C57BL/6 mice, represented by the decreased volume of oxygen consumption and heat production at the whole-body level.

CONCLUSION:

UCP3 protein was involved in the incidence of high-salt induced hypertension and the progression of cardiac dysfunction in the early stages of heart failure. UCP3 ablation exacerbated high-salt-induced cardiac hypertrophy and cardiac dysfunction.

KEYWORDS:

Cardiac hypertrophy; Elevated blood pressure; High salt; Uncoupling protein 3

PMID:
29694982
DOI:
10.1159/000489244
[Indexed for MEDLINE]
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