The DOI matches its Crossref record; 212 of the 213 references it cites were found in a registry or an index.
Cholesterol and Ion Channels
Open accessAbstract
A variety of ion channels, including members of all major ion channel families, have been shown to be regulated by changes in the level of membrane cholesterol and partition into cholesterol-rich membrane domains. In general, several types of cholesterol effects have been described. The most common effect is suppression of channel activity by an increase in membrane cholesterol, an effect that was described for several types of inwardly-rectifying K(+) channels, voltage-gated K(+) channels, Ca(+2) sensitive K(+) channels, voltage-gated Na(+) channels, N-type voltage-gated Ca(+2) channels and volume-regulated anion channels. In contrast, several types of ion channels, such as epithelial amiloride-sensitive Na(+) channels and Transient Receptor Potential channels, as well as some of the types of inwardly-rectifying and voltage-gated K(+) channels were shown to be inhibited by cholesterol depletion. Cholesterol was also shown to alter the kinetic properties and current-voltage dependence of several voltage-gated channels. Finally, maintaining membrane cholesterol level is required for coupling ion channels to signalling cascades. In terms of the mechanisms, three general mechanisms have been proposed: (i) specific interactions between cholesterol and the channel protein, (ii) changes in the physical properties of the membrane bilayer and (iii) maintaining the scaffolds for protein-protein interactions. The goal of this review is to describe systematically the role of cholesterol in regulation of the major types of ion channels and to discuss these effects in the context of the models proposed.
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“In addition to inhibiting ABCA1 function in cholesterol efflux, the biased membrane lipid composition potentially interferes with functions of several channels on the membrane directly or by altering bilayer stiffness and hydrophobic mismatch between transmembrane domains and the lipid bilayer69.”
From An iPSC-derived astrocyte model of fragile X syndrome exhibits dysregulated cholesterol homeostasis (2023) · cites this paper as [69]
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Items 201–213 of 213
Regulation of the cell swelling‐activated chloride conductance by cholesterol‐rich membrane domains
Lim, C. H., Schoonderwoerd, K. C., Kleijer, W. J., de Jonge, H. R., & Tilly, B. C. (2006) · Acta Physiologica · doi:10.1111/j.1748-1716.2006.01534.x · Cited by 23
Bovine and Mouse SLO3 K+ Channels
Santi, C. M., Butler, A., Kuhn, J., Wei, A. D., & Salkoff, L. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.015040 · Cited by 23
Mathew, V., & Lerman, A. (2001) · Atherosclerosis · doi:10.1016/s0021-9150(00)00493-7 · Cited by 20
Membrane Tension Modulates the Effects of Apical Cholesterol on the Renal Epithelial Sodium Channel
Wei, S., Li, X., Chou, C., Liang, Y., Peng, J., Warnock, D. G., & Ma, H.-P. (2007) · The Journal of Membrane Biology · doi:10.1007/s00232-007-9071-7 · Cited by 20
Du, P., Cui, G., Wang, Y., Zhang, X., Ma, K.-J., & Wei, J.-G. (2006) · Acta Biochimica et Biophysica Sinica · doi:10.1111/j.1745-7270.2006.00236.x · Cited by 19
Cholesterol Depletion and Genistein as Tools to Promote F508delCFTR Retention at the Plasma Membrane
Lim, C. H., Bijvelds, M. J. C., Nigg, A. L., Schoonderwoerd, K. C., Houtsmuller, A. B., de Jonge, H. R., & Tilly, B. C. (2007) · Cellular Physiology and Biochemistry · doi:10.1159/000107531 · Cited by 18
Ren, Y. J., Xu, X., Zhong, C. B., Feng, N., & Wang, X. (2001) · PubMed · Cited by 16
Porosome: the Universal Molecular Machinery for Cell Secretion
Jena, B. P. (2008) · Molecules and Cells · doi:10.1016/s1016-8478(23)14032-5 · Cited by 15
Cholesterol‐depleting compounds modulate K+‐currents in Drosophila Kenyon cells
Gasque, G., Labarca, P. P., & Darszon, A. (2005) · FEBS Letters · doi:10.1016/j.febslet.2005.08.022 · Cited by 13
Pongo, E., Balla, Z., Mubagwa, K., Flameng, W. J., Edes, I. F., Szilvassy, Z., & Ferdinándy, P. (2001) · European Journal of Pharmacology · doi:10.1016/s0014-2999(01)00954-2 · Cited by 13
Cheema, T. A., & Fisher, S. K. (2007) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.107.131110 · Cited by 13
Effects of treatment with 17β-estradiol on the hypercholesterolemic rabbit middle cerebral artery
Ghanam, K., Javellaud, J., Ea-Kim, L., & Oudart, N. (2000) · Maturitas · doi:10.1016/s0378-5122(00)00088-8 · Cited by 11
Down-regulation of endogenous nitric oxide synthase inhibitors on endothelial SK3 expression
Zhou, Z., Jiang, D., Jia, S., Xiao, H., Xiao, B., & Li, Y. (2007) · Vascular Pharmacology · doi:10.1016/j.vph.2007.08.003 · Cited by 4
Research works printed but not linked: 3
- Genda, S., Miura, T., Miki, T., Ichikawa, Y., and Shimamoto K., 2002, K(ATP) channel opening is an endogenous mechanism of protection against the no-reflow phenomenon but its function is compromised by hypercholesterolemia. J Am Coll Cardiol. 40: 1339–1346. · DOI
- Popp B, Schmid A, and Benz R., 1995, Role of sterols in the functional reconstitution of water-soluble mitochondrial porins from different organisms. Biochemistry. 34: 3352–3361. · DOI
- Zheng, Y.Z., Berg, K.B., and Foster, L.J., 2009, Mitochondria do not contain lipid rafts, and lipid rafts do not contain mitochondrial proteins. J Lipid Res. 50: 988–998. · DOI
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Sheng, R., Chen, Y., Yung Gee, H., Stec, E., Melowic, H. R., Blatner, N. R., Tun, M. P., Kim, Y., Källberg, M., Fujiwara, T. K., et al. (2012) · Nature Communications · doi:10.1038/ncomms2221 · Cited by 179
Brain cell type-specific cholesterol metabolism and implications for learning and memory
Li, D., Zhang, J., & Liu, Q. (2022) · Trends in Neurosciences · doi:10.1016/j.tins.2022.01.002 · Cited by 163
Cholesterol selectively activates canonical Wnt signalling over non-canonical Wnt signalling
Sheng, R., Kim, H., Lee, H., Xin, Y., Chen, Y., Tian, W., Cui, Y., Choi, J.-C., Doh, J., Han, J.-K., et al. (2014) · Nature Communications · doi:10.1038/ncomms5393 · Cited by 157
An iPSC-derived astrocyte model of fragile X syndrome exhibits dysregulated cholesterol homeostasis
Talvio, K., Wagner, V. A., Minkeviciene, R., Kirkwood, J. S., Kulinich, A. O., Umemori, J., Bhatia, A., Hur, M., Käkelä, R., Ethell, I. M., et al. (2023) · Communications Biology · doi:10.1038/s42003-023-05147-9 · Cited by 8
Metadata
- Authors
- Levitan, I., Fang, Y., Rosenhouse-Dantsker, A., & Romanenko, V.
- Affiliations
- University of Illinois Chicago (US)
- University of Pennsylvania (US)
- University of Rochester Medicine (US)
- Corresponding author
- Levitan, Irena
- Venue
- Subcellular Biochemistry
- Publisher
- Springer Netherlands
- Published
- 2010
- Volume
- 51
- Pages
- 509-549
- ISSN
- 0306-0225 (ISSN-L)
- PMC
- PMC2895485
- OpenAlex
- W1497754562
- Cited by
- 247
- References
- 213
- Citations by year
- 2026: 17 · 2025: 17 · 2024: 14 · 2023: 16 · 2022: 26 · 2021: 19 · 2020: 11 · 2019: 14 · 2018: 9 · 2017: 12 · 2016: 7 · 2015: 10 · 2014: 21 · 2013: 15 · 2012: 17
- FWCI
- 20.98
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Sub-cellular biochemistry/Subcellular biochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL073965, HL073965, R01HL083298, HL-083298)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Lipid Membrane Structure and Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Caveolin-1 and cellular processes
- Keywords
- membrane cholesterol, ion channel modulation, cholesterol-rich membrane domains, inwardly rectifying potassium channels, voltage-gated potassium channels, voltage-gated sodium channels, N-type calcium channels, volume-regulated anion channel, amiloride-sensitive sodium channel, TRP channels, cholesterol depletion, channel kinetics
- MeSH terms
- Animals, Cholesterol, Humans, Hypercholesterolemia, Ion Channels, Membrane Lipids, Molecular Conformation, Calcium Channels, Sodium Channels, Signal Transduction, Ion Channel Gating, Chloride Channels, Membrane Microdomains, Potassium Channels, Voltage-Gated, Potassium Channels, Inwardly Rectifying, Potassium Channels, Calcium-Activated, TRPC Cation Channels
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