Results 1 to 10 of about 143,705 (309)

Over expression of Plk1 does not induce cell division in rat cardiac myocytes in vitro. [PDF]

PLoS ONE, 2009
BACKGROUND:Mammalian cardiac myocytes withdraw from the cell cycle during post-natal development, resulting in a non-proliferating, fully differentiated adult phenotype that is unable to repair damage to the myocardium, such as occurs following a ...
Carmen H Coxon, Katrina A Bicknell, Fleur L Moseley, Gavin Brooks   +3 more
doaj   +1 more source

Down-regulation of replication factor C-40 (RFC40) causes chromosomal missegregation in neonatal and hypertrophic adult rat cardiac myocytes. [PDF]

PLoS ONE, 2012
BACKGROUND: Adult mammalian cardiac myocytes are generally assumed to be terminally differentiated; nonetheless, a small fraction of cardiac myocytes have been shown to replicate during ventricular remodeling.
Hirotaka Ata, Deepa Shrestha, Masahiko Oka, Rikuo Ochi, Chian Ju Jong, Sarah Gebb, John Benjamin, Stephen Schaffer, Holly H Hobart, James Downey, Ivan McMurtry, Rakhee Gupte   +11 more
doaj   +1 more source

Innate immune signaling in hearts and buccal mucosa cells of patients with arrhythmogenic cardiomyopathy

Heart Rhythm O2, 2023
Background: Nuclear factor κB (NF-κB) signaling in cardiac myocytes causes disease in a mouse model of arrhythmogenic cardiomyopathy (ACM) by mobilizing CCR2-expressing macrophages that promote myocardial injury and arrhythmias.
Carlos Bueno-Beti, PhD, Alessandro Tafuni, MD, Stephen P. Chelko, PhD, FHRS, Mary N. Sheppard, MD, Ella Field, MSc, Jennifer Tollit, MSc, Imogen K. Heenan, BSc, Annabelle Barnes, BSc, Matthew R. Taylor, MD, PhD, Luisa Mestroni, MD, Juan Pablo Kaski, MD, Jeffrey E. Saffitz, MD, PhD, FHRS, Angeliki Asimaki, PhD   +12 more
doaj   +1 more source

PARM-1 is an endoplasmic reticulum molecule involved in endoplasmic reticulum stress-induced apoptosis in rat cardiac myocytes. [PDF]

PLoS ONE, 2010
To identify novel transmembrane and secretory molecules expressed in cardiac myocytes, signal sequence trap screening was performed in rat neonatal cardiac myocytes.
Koji Isodono, Tomosaburo Takahashi, Hiroko Imoto, Naohiko Nakanishi, Takehiro Ogata, Satoshi Asada, Atsuo Adachi, Tomomi Ueyama, Hidemasa Oh, Hiroaki Matsubara   +9 more
doaj   +1 more source

Subcellular heterogeneity of ryanodine receptor properties in ventricular myocytes with low T-tubule density [PDF]

, 2011
Rationale: In ventricular myocytes of large mammals, not all ryanodine receptor (RyR) clusters are associated with T-tubules (TTs); this fraction increases with cellular remodeling after myocardial infarction (MI).
AM Gomez, AM Gomez, AR Lyon, AV Zima, AV Zima, AV Zima, AW Trafford, C Franzini-Armstrong, DJ Crossman, DJ Santiago, DR Scriven, EA Sobie, EA Sobie, F Brette, FR Heinzel, FR Heinzel, Frank R. Heinzel, Godfrey L. Smith, H Cheng, H Cheng, H Katoh, H Satoh, J Huser, JI Goldhaber, JJ Saucerman, JM Cordeiro, JR Lopez-Lopez, JW Bassani, K Acsai, K Toischer, KA Sheehan, Karin R. Sipido, KR Sipido, L Cleemann, L Mackenzie, Liesbeth Biesmans, M Volkers, Marcello Rota, Niall Macquaide, P Lipp, P Neco, PS Haddock, PS Shacklock, Q Song, RP Xiao, S Despa, S Seki, SH Woo, SH Woo, SV Meethal, TR Shannon, TR Shannon, V Lukyanenko, V Lukyanenko, Virginie Bito, WE Louch   +55 more
core   +12 more sources

Myocardial Mitochondrial DNA Drives Macrophage Inflammatory Response through STING Signaling in Coxsackievirus B3-Induced Viral Myocarditis

Cells, 2023
Coxsackievirus B3 (CVB3), a single-stranded positive RNA virus, primarily infects cardiac myocytes and is a major causative pathogen for viral myocarditis (VMC), driving cardiac inflammation and organ dysfunction.
Andong Qin, Zhenke Wen, Sidong Xiong
doaj   +1 more source

Epigenetic regulation of cardiac myocyte differentiation† [PDF]

Frontiers in Genetics, 2014
Cardiac myocytes (CMs) proliferate robustly during fetal life but withdraw permanently from the cell cycle soon after birth and undergo terminal differentiation. This cell cycle exit is associated with the upregulation of a host of adult cardiac-specific genes.
Oyama, Kyohei, El-Nachef, Danny, Zhang, Yiqiang, Sdek, Patima, MacLellan, W. Robb   +4 more
openaire   +3 more sources

A Comorbidity Model of Myocardial Ischemia/Reperfusion Injury and Hypercholesterolemia in Rat Cardiac Myocyte Cultures

Frontiers in Physiology, 2020
IntroductionThe use of comorbidity models is crucial in cardioprotective drug development. Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury.
András Makkos, Ágnes Szántai, János Pálóczi, Judit Pipis, Bernadett Kiss, Bernadett Kiss, Paola Poggi, Péter Ferdinandy, Péter Ferdinandy, Péter Ferdinandy, Alexandros Chatgilialoglu, Anikó Görbe, Anikó Görbe, Anikó Görbe   +13 more
doaj   +1 more source

High-Sensitive Cardiospecific Troponins: The Role of Gender-Specific Concentration in the Diagnosis of Acute Coronary Syndrome (Descriptive Review)

Reviews in Cardiovascular Medicine, 2023
Cardiospecific troponins are specifically localized in the troponin-tropomyosin complex and in the cytoplasm of cardiac myocytes. Cardiospecific troponin molecules are released from cardiac myocytes upon their death (irreversible damage in acute coronary
Aleksey Chaulin
doaj   +1 more source

Junctional sarcoplasmic reticulum motility in adult mouse ventricular myocytes. [PDF]

, 2020
Excitation-contraction (EC) coupling is the coordinated process by which an action potential triggers cardiac myocyte contraction. EC coupling is initiated in dyads where the junctional sarcoplasmic reticulum (jSR) is in tight proximity to the sarcolemma
de la Mata, Ana, Drum, Benjamin M, Grainger, Nathan, Grainger, Nathan, Santana, L Fernando, Yuan, Can   +5 more
core   +2 more sources