for Journals by Title or ISSN
for Articles by Keywords

Publisher: Smart Science and Technology LLC   (Total: 21 journals)   [Sort by number of followers]

Showing 1 - 21 of 21 Journals sorted alphabetically
Abdomen     Open Access  
Cancer Cell & Microenvironment     Open Access   (Followers: 10)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 8)
Immunoendocrinology     Open Access   (Followers: 1)
Inflammation and Cell Signaling     Open Access   (Followers: 3)
Itch & Pain     Open Access   (Followers: 2)
J. of Advanced Nutrition and Human Metabolism     Open Access   (Followers: 15)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 3)
Neurotransmitter     Open Access  
Precision Medicine     Open Access   (Followers: 2)
Receptors & Clinical Investigation     Open Access   (Followers: 1)
RNA & Disease     Open Access   (Followers: 1)
Science Proceedings     Open Access   (Followers: 1)
Stem Cell and Translational Investigation     Open Access   (Followers: 2)
Stem Cell Epigenetics     Open Access   (Followers: 3)
Telomere and Telomerase     Open Access  
Therapeutic Targets for Neurological Diseases     Open Access   (Followers: 1)
Uterus & Ovary     Open Access  
Similar Journals
Journal Cover
Cardiovascular Regenerative Medicine
Number of Followers: 0  

  This is an Open Access Journal Open Access journal
ISSN (Print) 2378-3141 - ISSN (Online) 2378-3141
Published by Smart Science and Technology LLC Homepage  [21 journals]
  • Signaling Mechanisms of the E3 Ligase Mule in the Heart

    • Authors: Filio Billia, Keith Dadson
      Abstract: The regulation of cardiac homeostasis is especially important in a non-regenerative cell type like the cardiomyocyte. Suppression of hypertrophic and apoptotic signaling pathways is of critical importance for the regulation of cardiac homeostasis. The ubiquitin-proteasomal system is a highly conserved cascade which plays an essential role in regulating a diversity of systems through the rapid post-translational protein modification leading to changes in protein signaling and stability. This system is also important in the cardiovascular system, and in particular, in the heart. In this review, we discuss what is known of the regulation of cardiac homeostasis by the E3 ubiquitin ligase Mule, who’s substrates include the highly characterized proteins p53, myc, and Mcl-1, which are known to play important roles in the regulation of apoptosis and cardiac hypertrophy in heart failure. Mule is also known to play various roles in the regulation of chromatin dynamics, especially following the detection of DNA double strand breaks, and the activation of the DNA damage response. Accordingly, Mule appears to play an indispensable role in the regulation of cardiac homeostasis.
      PubDate: 2017-09-04
      DOI: 10.14800/crm.1590
      Issue No: Vol. 4 (2017)
  • Classical and non-canonical functions of p53: Therapeutic opportunities
           for cardiac repair.

    • Authors: Shanna Stanley-Hasnain, Ludger Hauck, Filio Billia
      Abstract: Heart failure is the leading cause of morbidity and mortality worldwide. Adult cardiomyocytes are post-mitotic cells with a very low capacity to proliferate. The lack of significant regenerative potential renders the heart vulnerable to ischemic damage. After myocardial infarction, cardiomyocytes undergo maladaptive changes characterized by hypertrophic growth to compensate for loss of contractility. The existing armamentarium of conventional pharmacological therapy for heart failure can only slow the progression of the disease by alleviating the workload of the heart. Accumulating evidence has shown that the tumor suppressor p53 is an important factor in the development of heart failure and that its genetic ablation in mouse models exerts beneficial effects on heart function. Here, we consider the cross-talk between p53 and its downstream effectors at the hub of major biological processes that are relevant to cardiac biology.
      PubDate: 2017-08-14
      DOI: 10.14800/crm.1579
      Issue No: Vol. 4 (2017)
  • An emerging role for the Cdk-inhibitors p21Cip1/Waf1 and p27Kip1 as
           potential therapies for the treatment of cardiac hypertrophy.

    • Authors: Shanna Stanley-Hasnain, Ludger Hauck, Filio Billia
      Abstract: Heart failure is the leading cause of morbidity and mortality worldwide. Adult cardiomyocytes are post-mitotic cells that are substantially refractory to re-enter the cell cycle. This is exemplified by the absence of significant proliferative potential in differentiated cardiomyocytes. When exposed to aberrant growth stimuli, cardiomyocytes undergo maladaptive changes characterized by hypertrophic growth. The existing armamentarium of conventional pharmacological therapy can only slow the progression of the disease by alleviating the workload of the heart. Various agonist- and stress-induced extracellular signal transduction pathways could be target by novel agents for the treatment of pathological cardiac growth. Among these, the cyclin-dependent kinase inhibitors p21 and p27 have been recognized as potent inhibitors of apoptosis, growth and proliferation in cardiovascular disease. The role of the cell cycle factors p21 and p27 in the regulation of growth-associated processes in the heart, and their potential therapeutic implications are not immediately obvious, as it is the case in cardiovascular biology. In this review, we focus on the multiple functions of p21 and p27 in the regulation of hypertrophy, and briefly discuss pathways that play critical play therein. All these selected studies attest an important role of p21 and p27 in the regulation of hypertrophy in isolated rat cardiomyocytes, and in various genetic murine models of heart failure. The available evidence suggests that therapeutic clinical approaches involving p21 and p27 have the potential to to treat heart failure in patients. 
      PubDate: 2017-03-27
      DOI: 10.14800/crm.1527
      Issue No: Vol. 4 (2017)
  • p38 MAPK and the compromised regenerative response of the infarcted adult

    • Authors: Angelo Calderone
      Abstract: Mononucleated cardiomyocytes promoted the hyperplasic growth of the embryonic mammalian heart and the proliferative phenotype was retained by neonatal cardiomyocytes for a short duration after birth. Despite the cell cycle re-entry of pre-existing cardiomyocytes, regeneration of the damaged neonatal heart required the coordinated effort of reparative embryonic macrophages. During postnatal development, pre-existing cardiomyocytes underwent karyokinesis in the absence of cytokinesis and the ability to proliferate was lost. However, a paucity of mononucleated cardiomyocytes persisted in the adult heart and an ischemic insult facilitated re-entry into the cell cycle. The latter paradigm provided a semblance of hope that a cardiac regenerative response was possible. However, the selective expansion of pro-inflammatory monocyte-derived macrophages following ischemic injury to the adult heart may have further impeded an already compromised regenerative response. The serine/threonine kinase p38 MAPK was identified as a seminal target of pro-inflammatory cytokines and a smaller infarct was reported after inhibition. The smaller infarct was attributed in part to cardiac regeneration as p38 MAPK suppressed the cell cycle re-entry of neonatal/adult cardiomyocytes in response to peptide growth factors. p38 MAPK-mediated inhibition of cell cycle re-entry may be related in part to the attenuation of nestin expression by pre-existing cardiomyocytes as the intermediate filament protein was directly implicated in the cell proliferation of normal and tumorigenic cells. Thus, targeting the inflammatory response via p38 MAPK inhibition may represent a rational approach to unmask the proliferative potential of pre-existing mononucleated cardiomyocytes and initiate a partial regenerative response of the infarcted adult mammalian heart.
      PubDate: 2017-02-27
      DOI: 10.14800/crm.1508
      Issue No: Vol. 4 (2017)
  • MicroRNAs regulating Meis1 expression and inducing cardiomyocyte

    • Authors: Raghav Pandey, Yunhan Yang, Laeia Jackson, Rafeeq Habeebahmed
      Abstract: Cardiovascular disease has been the biggest killer in the United States for decades, with almost a million new cases each year. Even though mammalian rodent neonatal cardiomyocytes show proliferative potential for up to 5 days, adult cardiomyocytes lose this ability. Insufficient cardiomyocyte proliferation is one of the major reasons for the lack of regeneration of myocardial tissue, post injury. Several studies have looked at the mechanisms responsible for the arrest in proliferation at an adult stage. Following up on a recent study by Eulalio et al’s study on functional screening of 875 miRNAs for neonatal cardiomyocyte proliferation, we recently identified several miRNAs that induce proliferation in naturally senescent adult cardiomyocytes. Additional studies by Mahmood et al 2013 have identified Meis1 as the major regulator of cardiomyocyte cell cycle. In our present study we have identified three of the adult cardiomyocyte proliferation inducing miRNAs to have binding sites on the 3’UTR of Meis1 gene by in-silico analysis and luciferase assay. Additionally we found these miRNAs; miR-548c-3p, miR-509-3p, and miR-23b-3p to induce significant proliferation in adult cardiomyocytes through translational inhibition of Meis1. We found a significant increase in the number of ACMs with each miRNA, in combination, and with siRNA mediated inhibition of Meis1 gene. We confirmed that these microRNAs, through inhibition of Meis1, affect its downstream targets and thereby regulate cell-cycle progression. Further investigating of the mechanism of action of these miRNAs can identify other treatment options for abnormalities associated with the lack of cardiac regeneration post myocardial injury. 
      PubDate: 2016-12-19
      DOI: 10.14800/crm.1468
      Issue No: Vol. 3 (2016)
  • Induced Pluripotent Stem Cell and Its Derivatives in Ischemic Heart

    • Authors: Lingling Chang, Samuel C. Dudley, Yi Zhun
      Abstract: Ischemic heart disease (IHD) is the leading cause of morbidity and disease burden worldwide. However, traditional interventions could not well improve this situation. Stem cell therapy is a promising strategy, and induced pluripotent stem cell (iPSC) represents a potential candidate superior to embryonic stem cell in spite of cell source and ethical concerns. Herein, we provide an overview of cardiac differentiation of iPSC and its role in IHD including myocardial infarction and ischemic heart failure. After this, the existing problems in current iPSC field will get analyzed, hoping to provide some enlightenment for iPSC research.  
      PubDate: 2016-09-19
      DOI: 10.14800/crm.1425
      Issue No: Vol. 3 (2016)
  • Sarcolipin in atrium-specific gene targeting

    • Authors: Daisuke Shimura, Atsushi Nakano, Susumu Minamisawa
      Abstract: The timely expression of transcriptional factors in a specific localization, which determines the cell’s fate, is critical to proper heart development. The Cre/loxP site-specific gene-targeting technique has contributed to the analysis of the functions of these transcriptional factors in the field of cardiovascular research. To analyze the role of certain genes more precisely, heart-specific gene targeting and chamber-specific gene targeting is needed, because the atrium and the ventricle of the heart have their own function, structure, gene expression, and even metabolic profile. In this review, we focused on sarcolipin (SLN), which is expressed in an atrium-specific manner. We generated an SlnCre/+ mouse line by inserting Cre into the endogenous SLN locus by homologous recombination. Since SlnCre/+ mice show a normal morphological and functional phenotype in the heart, SlnCre/+ can be utilized for atrium-specific gene targeting to clarify the mechanisms of atrial development and pathogenesis. Understanding the precise mechanisms of heart development is also required to enable regenerative medicine to advance and induce proper atrial and/or ventricular myocytes. Here, we summarize the SLN function in the atrium, the phenotype in the SlnCre/+ mouse atria we observed, and the future prospects of atrium-specific gene targeting.
      PubDate: 2016-05-23
      DOI: 10.14800/crm.1297
      Issue No: Vol. 3 (2016)
  • Doxorubicin-induced cardiomyopathy: An update beyond oxidative stress and
           myocardial cell death

    • Authors: Paiboon Jungsuwadee
      Abstract: The clinical use of doxorubicin is limited by the total cumulative dose due to its dose-related cardiac toxicities. Clinical manifestation of doxorubicin-mediated cardiotoxicity may be presented in forms of arrhythmia, cardiomyopathy, or congestive heart failure. Cardiomyopathy is a condition in which the cardiac muscles are damaged, leading to cardiac dysfunctions. Mechanistically, the damage of cardiomyocytes is believed to be mediated primarily by oxidative stress. Cardiac mitochondrial damage is evident within a few hours following exposure to doxorubicin. When cardiomyocytes are chronically exposed to doxorubicin, the damages are even more pronounced. In animal models of doxorubicin-induced cardiotoxicity, lacking multidrug-resistance associated protein 1 intensifies damage of the cardiac nuclei and causes more severe left ventricular dysfunction. It appears that cardiac tissue damage induced by doxorubicin is not confined to cardiomyocytes; endothelial cells are affected by doxorubicin as well. Current evidence has indicated that there is a cross-talk between endothelial cells and cardiomyocytes. The purpose of this article is to briefly review and update the current findings associated with doxorubicin-induced cardiomyopathy.
      PubDate: 2016-01-12
      DOI: 10.14800/crm.1127
      Issue No: Vol. 3 (2016)
School of Mathematical and Computer Sciences
Heriot-Watt University
Edinburgh, EH14 4AS, UK
Tel: +00 44 (0)131 4513762
Fax: +00 44 (0)131 4513327
Home (Search)
Subjects A-Z
Publishers A-Z
Your IP address:
About JournalTOCs
News (blog, publications)
JournalTOCs on Twitter   JournalTOCs on Facebook

JournalTOCs © 2009-