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Bito, V; Heinzel, FR; Biesmans, L; Antoons, G; Sipido, KR.
Crosstalk between L-type Ca2+ channels and the sarcoplasmic reticulum: alterations during cardiac remodelling.
Cardiovasc Res. 2008; 77(2): 315-324. Doi: 10.1093/cvr/cvm063 [OPEN ACCESS]
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Co-Autor*innen der Med Uni Graz
Antoons Gudrun
Heinzel Frank
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Abstract:
In the cardiac dyad, sarcolemmal L-type Ca(2+) channels (LCCs) and sarcoplasmic reticulum (SR) Ca(2+) release channels (RyR) are structurally in close proximity. This organization provides for an efficient functional coupling, tuning SR Ca(2+) release for optimal contraction of the myocyte. Given that LCC are regulated by the prevailing [Ca(2+)], this structural organization is the setting for feedback mechanisms and crosstalk. A defective coupling of Ca(2+) influx via LCC to activation of RyR has been implicated in reduced SR Ca(2+) release in heart failure. Both functional changes in LCC properties and structural re-organization of LCC in T-tubules could be involved. LCC are regulated by cytosolic Ca(2+), and crosstalk with SR Ca(2+) handling occurs on a long-term basis, i.e. during steady-state changes in heart rate, on an intermediate-term basis, i.e. on a beat-to-beat basis during sudden rate changes, and on a very short- or immediate-term basis, i.e. during a single heartbeat. We review the properties and consequences of these different feedback mechanisms and the changes in heart failure and cardiac hypertrophy that have thus far been studied.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Arrhythmias, Cardiac - etiology
Calcium - metabolism
Calcium Channels, L-Type - physiology
Cardiomegaly - metabolism
Feedback, Physiological -
Heart Failure - metabolism
Heart Rate -
Humans -
Myocardial Contraction -
Ryanodine Receptor Calcium Release Channel - physiology
Sarcoplasmic Reticulum - physiology

Find related publications in this database (Keywords)
cardiac hypertrophy
heart failure
calcium channel
sarcoplasmic reticulum
excitation-contraction coupling
arrhythmias
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