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Zinc ameliorates human aortic valve calcification through GPR39 mediated ERK1/2 signalling pathway
Ziying Chen1, Flora Gordillo-Martinez1, Lei Jiang2
1Guangzhou Institute of Cardiovascular Disease, Guangdong Key Laboratory of Vascular Diseases, State Key Laboratory of Respiratory Disease, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510260, China.
Cardiovascular Research
|April 8, 2020
Summary
Zinc supplementation inhibits calcific aortic valve disease (CAVD) by reducing cell death and bone formation. This study highlights zinc transporters ZIP13 and ZIP14 as key regulators in CAVD progression.
Area of Science:
- Cardiovascular Research
- Mineral Metabolism
- Cell Biology
Background:
- Calcific aortic valve disease (CAVD) is a prevalent heart valve condition.
- Zinc accumulation is observed in calcified aortic valves, but its role is unclear.
Purpose of the Study:
- To investigate the direct role of zinc in the pathogenesis of CAVD.
- To explore zinc's potential as a therapeutic agent for CAVD.
Main Methods:
- Utilized a human valve interstitial cell (hVIC) calcification model.
- Analyzed human aortic valve tissues and patient blood samples.
- Investigated the GPR39 signaling pathway and zinc transporters ZIP13/ZIP14.
Main Results:
- Zinc supplementation (20 μM) reduced hVIC calcification, apoptosis, and osteogenic differentiation.
- Reduced GPR39 expression and serum zinc levels were found in CAVD patients and tissues.
- Zinc treatment restored GPR39 levels; ZIP13/ZIP14 upregulation mediated zinc's effects.
Conclusions:
- Zinc acts as a novel inhibitor of CAVD.
- ZIP13 and ZIP14 are critical regulators of hVIC calcification and osteogenic differentiation.
- Zinc supplementation presents a potential therapeutic strategy for CAVD.
