Long term regulation of cardiac l-type calcium channel by small G proteins

J. Magyar, Á Jenes, K. Kistamás, F. Ruzsnavszky, P. P. Nánási, J. Satin, N. Szentandrássy, T. Bányász

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Calcium ions are crucial elements of excitation-contraction coupling in cardiac myocytes. The intracellular Ca 2+ concentration changes continously during the cardiac cycle, but the Ca 2+ entering to the cell serves as an intracellular second messenger, as well. The Ca 2+ as a second messenger influences the activity of many intracellular signalling pathways and regulates gene expression. In cardiac myocytes the major pathway for Ca 2+ entry into cells is L-type calcium channel (LTCC). The precise control of LTCC function is essential for maintaining the calcium homeostasis of cardiac myocytes. Dysregulation of LTCC may result in different diseases like cardiac hypertrophy, arrhytmias, heart failure. The physiological and pathological structural changes in the heart are induced in part by small G proteins. These proteins are involved in wide spectrum of cell biological functions including protein transport, regulation of cell proliferation, migration, apoptosis, and cytoskeletal rearrangement. Understanding the crosstalk between small G proteins and LTCC may help to understand the pathomechanism of different cardiac diseases and to develop a new generation of genetically-encoded Ca 2+ channel inhibitors.

Original languageEnglish
Pages (from-to)3714-3719
Number of pages6
JournalCurrent Medicinal Chemistry
Volume18
Issue number24
DOIs
StatePublished - Aug 2011

Funding

FundersFunder number
National Heart, Lung, and Blood Institute (NHLBI)R01HL074091

    Keywords

    • Calcium channel
    • Heart
    • Small G protein

    ASJC Scopus subject areas

    • Biochemistry
    • Molecular Medicine
    • Pharmacology
    • Drug Discovery
    • Organic Chemistry

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