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Adult Cardiomyocyte turnover

Eniko Lázár, Hesham A Sadek, Olaf Bergmann
The capacity of the mammalian heart to regenerate cardiomyocytes has been debated over the last decades. However, limitations in existing techniques to track and identify nascent cardiomyocytes have often led to inconsistent results. Radiocarbon (14C) birth dating, in combination with other quantitative strategies, allows to establish the number and age of human cardiomyocytes, making it possible to describe their age distribution and turnover dynamics. Accurate estimates of cardiomyocyte generation in the adult heart can provide the foundation for novel regenerative strategies that aim to stimulate cardiomyocyte renewal in various cardiac pathologies...
August 7, 2017: European Heart Journal
Shengnan Liu, Ya-Ping Jiang, Lisa M Ballou, Wei-Xing Zong, Richard Z Lin
Receptors that activate the heterotrimeric G protein Gαq are thought to play a role in the development of heart failure. Dysregulation of autophagy occurs in some pathological cardiac conditions including heart failure, but whether Gαq is involved in this process is unknown. We used a cardiomyocyte-specific transgenic mouse model of inducible Gαq activation (termed GαqQ209L) to address this question. After 7 days of Gαq activation, GαqQ209L hearts contained more autophagic vacuoles than wild type hearts...
April 2017: Journal of Cardiovascular Pharmacology
M Pásek, J Šimurda, G Christé
The ratio of densities of Na-Ca exchanger current (INaCa) in the t-tubular and surface membranes (INaCa-ratio) computed from the values of INaCa and membrane capacitances (Cm) measured in adult rat ventricular cardiomyocytes before and after detubulation ranges between 1.7 and 25 (potentially even 40). Variations of action potential waveform and of calcium turnover within this span of the INaCa-ratio were simulated employing previously developed model of rat ventricular cell incorporating separate description of ion transport systems in the t-tubular and surface membranes...
2017: BioMed Research International
Ravi Karra, Kenneth D Poss
Heart failure is a major source of morbidity and mortality. Replacing lost myocardium with new tissue is a major goal of regenerative medicine. Unlike adult mammals, zebrafish and neonatal mice are capable of heart regeneration following cardiac injury. In both contexts, the regenerative program echoes molecular and cellular events that occur during cardiac development and morphogenesis, notably muscle creation through division of cardiomyocytes. Based on studies over the past decade, it is now accepted that the adult mammalian heart undergoes a low grade of cardiomyocyte turnover...
February 1, 2017: Journal of Clinical Investigation
Qi Xiao, Guoxin Zhang, Huijuan Wang, Lai Chen, Shuangshuang Lu, Dejing Pan, Geng Liu, Zhongzhou Yang
In the field of heart regeneration, the proliferative potential of cardiomyocytes in postnatal mice is under intense investigation. However, solely relying on immunostaining of proliferation markers, the long-term proliferation dynamics and potential of the cardiomyocytes cannot be readily addressed. Previously, we found that a p53 promoter-driving reporter predominantly marked the proliferating lineages in mice. Here, we established a p53 -based genetic tracing system to investigate postnatal cardiomyocyte proliferation and heart regeneration...
February 15, 2017: Development
Waleed M Elhelaly, Nicholas T Lam, Mohamed Hamza, Shuda Xia, Hesham A Sadek
Heart failure is a costly and deadly disease, affecting over 23 million patients worldwide, half of which die within 5 years of diagnosis. The pathophysiological basis of heart failure is the inability of the adult heart to regenerate lost or damaged myocardium. Although limited myocyte turnover does occur in the adult heart, it is insufficient for restoration of contractile function (Nadal-Ginard, 2001; Laflamme et al., 2002; Quaini et al., 2002; Hsieh et al., 2007; Bergmann et al., 2009, 2012). In contrast to lower vertebrates (Poss et al...
2016: Frontiers in Cell and Developmental Biology
Evan Graham, Olaf Bergmann
Regenerative mechanisms reported in the hearts of lower vertebrates have been recapitulated in the mammalian milieu, and recent studies have provided strong evidence for cardiomyocyte turnover in humans. These findings speak to an emerging consensus that adult mammalian cardiomyocytes do have the ability to divide, and it stands to reason that enrichment of this innate proliferative capacity should prove essential for complete cardiac regeneration.
January 2017: Physiology
Raife Dilek Turan, Galip Servet Aslan, Doğacan Yücel, Remziye Döğer, Fatih Kocabaş
Heart has long been considered a terminally differentiated organ. Recent studies, however, have suggested that there is a modest degree of cardiomyocyte (CM) turnover in adult mammalian heart, albeit not sufficient for replacement of lost CMs following cardiac injuries. Cardiac regeneration studies in various model organisms including zebrafish, newt, and more recently in neonatal mouse, have demonstrated that CM dedifferentiation and concomitant proliferation play important roles in replacement of lost CMs and restoration of cardiac contractility...
November 2016: Anatolian Journal of Cardiology
M S W Xiang, K Kikuchi
Zebrafish possess a remarkable capacity for cardiac regeneration throughout their lifetime, providing a model for investigating endogenous cellular and molecular mechanisms regulating myocardial regeneration. By contrast, adult mammals have an extremely limited capacity for cardiac regeneration, contributing to mortality and morbidity from cardiac diseases such as myocardial infarction and heart failure. However, the viewpoint of the mammalian heart as a postmitotic organ was recently revised based on findings that the mammalian heart contains multiple undifferentiated cell types with cardiogenic potential as well as a robust regenerative capacity during a short period early in life...
2016: International Review of Cell and Molecular Biology
Konstantinos Malliaras, Styliani Vakrou, Chris J Kapelios, John N Nanas
INTRODUCTION: The -once viewed as heretical- concept of the adult mammalian heart as a dynamic organ capable of endogenous regeneration has recently gained traction. However, estimated rates of myocyte turnover vary wildly and the underlying mechanisms of cardiac plasticity remain controversial. It is still unclear whether the adult mammalian heart gives birth to new myocytes through proliferation of resident myocytes, through cardiomyogenic differentiation of endogenous progenitors or through both mechanisms...
November 2016: Expert Opinion on Biological Therapy
Liliana Kiczak, Alicja Tomaszek, Urszula Pasławska, Jacek Bania, Agnieszka Noszczyk-Nowak, Piotr Skrzypczak, Robert Pasławski, Maciej Zacharski, Adrian Janiszewski, Piotr Kuropka, Piotr Ponikowski, Ewa A Jankowska
BACKGROUND: Although sex differences in heart failure (HF) prevalence and severity have been recognized, its molecular mechanisms are poorly understood. We used a tachycardia-induced cardiomyopathy model to determine the sex specific remodeling pattern in male and female adult pigs. METHODS: We compared the echocardiographic and molecular measures of myocardial remodeling in 19 male and 12 female pigs with chronic symptomatic systolic HF due to right ventricle (RV) pacing (170 bpm) and 6 male and 5 female sham-operated controls...
2015: Biology of Sex Differences
Lauren Drowley, Chad Koonce, Samantha Peel, Anna Jonebring, Alleyn T Plowright, Steven J Kattman, Henrik Andersson, Blake Anson, Bradley J Swanson, Qing-Dong Wang, Gabriella Brolen
Several progenitor cell populations have been reported to exist in hearts that play a role in cardiac turnover and/or repair. Despite the presence of cardiac stem and progenitor cells within the myocardium, functional repair of the heart after injury is inadequate. Identification of the signaling pathways involved in the expansion and differentiation of cardiac progenitor cells (CPCs) will broaden insight into the fundamental mechanisms playing a role in cardiac homeostasis and disease and might provide strategies for in vivo regenerative therapies...
February 2016: Stem Cells Translational Medicine
Iñigo Valiente-Alandi, Carmen Albo-Castellanos, Diego Herrero, Elvira Arza, Maria Garcia-Gomez, José C Segovia, Mario Capecchi, Antonio Bernad
INTRODUCTION: The mammalian adult heart maintains a continuous, low cardiomyocyte turnover rate throughout life. Although many cardiac stem cell populations have been studied, the natural source for homeostatic repair has not yet been defined. The Polycomb protein BMI1 is the most representative marker of mouse adult stem cell systems. We have evaluated the relevance and role of cardiac Bmi1 (+) cells in cardiac physiological homeostasis. METHODS: Bmi1 (CreER/+);Rosa26 (YFP/+) (Bmi1-YFP) mice were used for lineage tracing strategy...
October 26, 2015: Stem Cell Research & Therapy
Jesse Macadangdang, Xuan Guan, Alec S T Smith, Rachel Lucero, Stefan Czerniecki, Martin K Childers, David L Mack, Deok-Ho Kim
Human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) offer unprecedented opportunities to study inherited heart conditions in vitro, but are phenotypically immature, limiting their ability to effectively model adult-onset diseases. Cardiomyopathy is becoming the leading cause of death in patients with Duchenne muscular dystrophy (DMD), but the pathogenesis of this disease phenotype is not fully understood. Therefore, we aimed to test whether biomimetic nanotopography could further stratify the disease phenotype of DMD hiPSC-CMs to create more translationally relevant cardiomyocytes for disease modeling applications...
September 2015: Cellular and Molecular Bioengineering
Arun Sharma, Sean M Wu
A low level of cardiomyocyte turnover occurs in the adult mammalian heart, but the source of these new cells remains unknown. Kimura et al., 2015 utilized a novel hypoxia-induced fate mapping system to identify a rare population of adult cardiomyocytes undergoing cell-cycle entry and expansion in healthy adult hearts and following ischemic injury.
September 1, 2015: Cell Metabolism
Konstantinos E Hatzistergos, Ellena C Paulino, Raul A Dulce, Lauro M Takeuchi, Michael A Bellio, Shathiyah Kulandavelu, Yenong Cao, Wayne Balkan, Rosemeire M Kanashiro-Takeuchi, Joshua M Hare
BACKGROUND: Mammalian heart regenerative activity is lost before adulthood but increases after cardiac injury. Cardiac repair mechanisms, which involve both endogenous cardiac stem cells (CSCs) and cardiomyocyte cell-cycle reentry, are inadequate to achieve full recovery after myocardial infarction (MI). Mice deficient in S-nitrosoglutathione reductase (GSNOR(-⁄-)), an enzyme regulating S-nitrosothiol turnover, have preserved cardiac function after MI. Here, we tested the hypothesis that GSNOR activity modulates cardiac cell proliferation in the post-MI adult heart...
July 2015: Journal of the American Heart Association
Gunes Ozhan, Gilbert Weidinger
The ability to repair damaged or lost tissues varies significantly among vertebrates. The regenerative ability of the heart is clinically very relevant, because adult teleost fish and amphibians can regenerate heart tissue, but we mammals cannot. Interestingly, heart regeneration is possible in neonatal mice, but this ability is lost within 7 days after birth. In zebrafish and neonatal mice, lost cardiomyocytes are regenerated via proliferation of spared, differentiated cardiomyocytes. While some cardiomyocyte turnover occurs in adult mammals, the cardiomyocyte production rate is too low in response to injury to regenerate the heart...
2015: Cell Regeneration
Wataru Kimura, Feng Xiao, Diana C Canseco, Shalini Muralidhar, SuWannee Thet, Helen M Zhang, Yezan Abderrahman, Rui Chen, Joseph A Garcia, John M Shelton, James A Richardson, Abdelrahman M Ashour, Aroumougame Asaithamby, Hanquan Liang, Chao Xing, Zhigang Lu, Cheng Cheng Zhang, Hesham A Sadek
Although the adult mammalian heart is incapable of meaningful functional recovery following substantial cardiomyocyte loss, it is now clear that modest cardiomyocyte turnover occurs in adult mouse and human hearts, mediated primarily by proliferation of pre-existing cardiomyocytes. However, fate mapping of these cycling cardiomyocytes has not been possible thus far owing to the lack of identifiable genetic markers. In several organs, stem or progenitor cells reside in relatively hypoxic microenvironments where the stabilization of the hypoxia-inducible factor 1 alpha (Hif-1α) subunit is critical for their maintenance and function...
July 9, 2015: Nature
Xing Yin, Lian Hu, Hao Feng, Lazar Z Krsmanovic, Kevin J Catt
Fetal cardiomyocytes have been utilized in studies on myocardial repair in the damaged hearts of rodents and other species. Changes in angiotensin II (Ang II) receptor expression, especially decline of its type II receptor (AT2), are known to occur during the growth of cardiomyocytes from fetus to adult. However, the extent to which changes in the signaling pathways of Ang II type I (AT1) and AT2 receptors via p42/44 mitogen-activated protein kinase (ERK1/2) activation affect the physiological and pathophysiological functions in cardiomyocytes has not been defined...
August 1, 2010: Hormone Molecular Biology and Clinical Investigation
Alexandra Raulf, Hannes Horder, Laura Tarnawski, Caroline Geisen, Annika Ottersbach, Wilhelm Röll, Stefan Jovinge, Bernd K Fleischmann, Michael Hesse
Even though the mammalian heart has been investigated for many years, there are still uncertainties in the fields of cardiac cell biology and regeneration with regard to exact fractions of cardiomyocytes (CMs) at different developmental stages, their plasticity after cardiac lesion and also their basal turnover rate. A main shortcoming is the accurate identification of CM and the demonstration of CM division. Therefore, an in vivo model taking advantage of a live reporter-based identification of CM nuclei and their cell cycle status is needed...
May 2015: Basic Research in Cardiology
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