期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 14, 期 7, 页码 1275-1288出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2010.3359
关键词
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资金
- Bundesministerium fur Bildung und Forschung (BMBF)
- Europaischer Fonds fur Regionalentwicklung (EFRE)
- Land Sachsen-Anhalt
The intracellular free calcium concentration subserves complex signaling roles in brain. Calcium cations (Ca2+) regulate neuronal plasticity underlying learning and memory and neuronal survival. Homo-and heterocellular control of Ca2+ homeostasis supports brain physiology maintaining neural integrity. Ca2+ fluxes across the plasma membrane and between intracellular organelles and compartments integrate diverse cellular functions. A vast array of checkpoints controls Ca2+, like G protein-coupled receptors, ion channels, Ca2+ binding proteins, transcriptional networks, and ion exchangers, in both the plasma membrane and the membranes of mitochondria and endoplasmic reticulum. Interactions between Ca2+ and reactive oxygen species signaling coordinate signaling, which can be either beneficial or detrimental. In neurodegenerative disorders, cellular Ca2+-regulating systems are compromised. Oxidative stress, perturbed energy metabolism, and alterations of disease-related proteins result in Ca2+-dependent synaptic dysfunction, impaired plasticity, and neuronal demise. We review Ca2+ control processes relevant for physiological and pathophysiological conditions in brain tissue. Dysregulation of Ca2+ is decisive for brain cell death and degeneration after ischemic stroke, long-term neurodegeneration in Alzheimer's disease, Parkinson's disease, Huntington's disease, inflammatory processes, such as in multiple sclerosis, epileptic sclerosis, and leucodystrophies. Understanding the underlying molecular processes is of critical importance for the development of novel therapeutic strategies to prevent neurodegeneration and confer neuroprotection. Antioxid. Redox Signal. 14, 1275-1288.
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