期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 8, 期 9-10, 页码 1707-1721出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2006.8.1707
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资金
- NHLBI NIH HHS [R01 HL77390-01] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL077390] Funding Source: NIH RePORTER
Zinc plays a vital role in various cellular functions. Zinc deprivation is associated with severe disorders related to growth, maturation, and stress responses. In the heart, zinc affects differentiation and regeneration of cardiac muscle, cardiac conductance, acute stress responses, and recovery of heart transplants. Recent discoveries of the molecular players in zinc homeostasis revealed that the amount of intracellular free zinc is tightly controlled on the level of uptake, intracellular sequestration, redistribution, storage, and elimination, consequently creating a narrow window of optimal zinc concentration in the cells. Most of intracellular zinc is bound to numerous structural and regulatory proteins, with metabolically active, labile zinc present in picoto nanomolar concentrations. The central position of zinc in the redox signaling network is built on its unique chemical nature. The redox inert zinc creates a redox active environment when it binds to a sulfur ligand. The reversible oxidation of the sulfur ligand is coupled to the reversible zinc release from the protein, thereby executing the task of so-called protein redox zinc switch. Clearly, the impairment of zinc homeostasis will have far reaching physiological consequences.
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