Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2005 Mar;125(3):249-52.
doi: 10.1085/jgp.200509268.

Modulation of cardiac function: titin springs into action

Chee Chew Lim  1 , Douglas B Sawyer
Affiliations
Review

Modulation of cardiac function: titin springs into action

Chee Chew Lim et al. J Gen Physiol. 2005 Mar.
No abstract available

PubMed Disclaimer

Figures

F<sc>igure</sc> 1.
Figure 1.
Excitation–contraction (EC) coupling and the response to β-adrenergic receptor (β-AR) stimulation. (A) EC coupling involves depolarization of the transverse tubule that activates voltage-gated L-type calcium channels (LTCC). Influx of calcium through LTCC triggers a greater calcium release from the SR into the cytoplasm via ryanodine receptor (RyR) channels, which activates contraction. Relaxation occurs when cytoplasmic calcium is resequestered by the SR calcium-ATPase (SERCA2a), which is regulated by phospholamban (PLB). The excess calcium that entered the cell via the LTCCs is eventually extruded by the sarcolemmal sodium/calcium exchanger (NCX). (B) β-AR stimulation involves binding of epinephrine and norepinephrine to the receptor, G protein–mediated activation of adenylate cyclase (AC), synthesis of cyclic AMP (cAMP), and activation of PKA. PKA-dependent phosphorylation of calcium handling and myofilament proteins are depicted in red. Asterisk denotes potential modulation of titin spring constant by calcium and/or calcium/S100A1. The overall effect of PKA phosphorylation is an augmentation in myocardial inotropy and lusitropy.
See this image and copyright information in PMC

Comment on

References

    1. Bers, D.M. 2002. Cardiac excitation-contraction coupling. Nature. 415:198–205. - PubMed
    1. Cazorla, O., A. Freiburg, M. Helmes, T. Centner, M. McNabb, Y. Wu, K. Trombitas, S. Labeit, and H. Granzier. 2000. Differential expression of cardiac titin isoforms and modulation of cellular stiffness. Circ. Res. 86:59–67. - PubMed
    1. Freiburg, A., K. Trombitas, W. Hell, O. Cazorla, F. Fougerousse, T. Centner, B. Kolmerer, C. Witt, J.S. Beckmann, C.C. Gregorio, et al. 2000. Series of exon-skipping events in the elastic spring region of titin as the structural basis for myofibrillar elastic diversity. Circ. Res. 86:1114–1121. - PubMed
    1. Fujita, H., D. Labeit, B. Gerull, S. Labeit, and H.L. Granzier. 2004. Titin isoform-dependent effect of calcium on passive myocardial tension. Am. J. Physiol. Heart Circ. Physiol. 287:H2528–H2534. - PubMed
    1. Fukuda, N., P. Nair, Y. Wu, and H. Granzier. 2005. Phosphorylation of titin modulates passive stiffness cardiac muscle in a titin isoform–dependent manner. J. Gen. Physiol. 125:257–271. - PMC - PubMed

Publication types