cardiac muscle

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Related to Cardiac myocytes: cardiac hypertrophy, Cardiomyocytes
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  • noun

Synonyms for cardiac muscle

References in periodicals archive ?
Evidence that human cardiac myocytes divide after myocardial infarction.
In cardiac myocytes, the contractile cycle of myofilaments is initiated in the systolic stage by Ca [sup]2+ entering the cytosol via voltage-activated L-type Ca [sup]2+ channels, such as dihydropyridine receptor, such Ca [sup]2+ ions will then bind the RyRs in the SR, and trigger the release of Ca [sup]2+ into cytosol from the SR, allowing binding to calmodulin (CAM) and activating the contractions of cardiac myocytes.
Also, due to similarities between cardiac myocytes, care should be taken with its use in humans.
Qu, "Complex darly and delayed afterdepolarization dynamics caused by voltage-calcium coupling in cardiac myocytes," Biophysical Journal, vol.
The H9c2 cardiomyoblast line shows different phenotype even from neonatal and adult cardiac myocytes, and additionally spontaneous electric activity and sarcomeric structure cannot be observed in them [28].
Sadek's discovery points to a novel mechanism of cell-cycle control in cardiac myocytes and lends credence to the potential for regenerating--rebuilding--the diseased heart.
In the present study, we investigated the rapid impact of low-dose BPS on rodent hearts and cardiac myocytes, with
LPS can stimulate cardiac myocytes to release TNF-alpha and nitric oxide to induce apoptosis via an autocrine manner, but this level of damage occurs in the microgram/ml range.
3] enters cardiac myocytes, combines with its receptors, and enters the nucleus, causing enhanced transcription of genes for a-myosin heavy chain ([alpha]-MHC), [beta]-adrenergic receptors, and [Na.
Hypotheses have been proposed for the pathogenesis of HCM and include suggestions that causal DNA mutations give rise to structural alterations in proteins that cause various stresses on cardiac myocytes.
Nitric oxide-dependent parasympathetic signaling is due to activation of constitutive endothelial (type III) nitric oxide synthase in cardiac myocytes.
Proponents of the CK-MB assay argue that CK-MB is released earlier from damaged cardiac myocytes than troponin is and that the assay is useful in cases of 'false-positive' troponin elevation such as renal failure or cardiac myopathies.
But now a research team lead by Parker has identified a set of 64 crucial parameters from more than 1,000 by which to judge stem cell derived cardiac myocytes.
Troponin I and T proteins are specific to cardiac myocytes and, unlike CK-MB, aren't elevated by damage to skeletal muscle.