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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: 9)
Cardiovascular Regenerative Medicine     Open Access  
Evidence-based Medicine & Public Health     Open Access   (Followers: 7)
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: 14)
Macrophage     Open Access  
Molecular & Cellular Epilepsy     Open Access   (Followers: 2)
Musculoskeletal Regeneration     Open Access   (Followers: 2)
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  
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
           heart

    • 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
           proliferation

    • 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
           Disease

    • 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)
       
  • Inhaled matters of the Heart

    • Authors: Ahmed Zaky, Aftab Ahmad, Louis J Dell'Italia, Leila Jahromi, Lee Ann Riesenberg, Sadis Matalon, Shama Ahmad
      Abstract: Inhalations of atmospheric pollutants, especially particulate matters, are known to cause severe cardiac effects and to exacerbate preexisting heart disease. Heart failure is an important sequellae of gaseous inhalation such as that of carbon monoxide. Similarly, other gases such as sulphur dioxide are known to cause detrimental cardiovascular events. However, mechanisms of these cardiac toxicities are so far unknown. Increased susceptibility of the heart to oxidative stress may play a role. Low levels of antioxidants in the heart as compared to other organs and high levels of reactive oxygen species produced due to the high energetic demand and metabolic rate in cardiac muscle are important in rendering this susceptibility. Acute inhalation of high concentrations of halogen gases is often fatal. Severe respiratory injury and distress occurs upon inhalation of halogens gases, such as chlorine and bromine; however, studies on their cardiac effects are scant. We have demonstrated that inhalation of high concentrations of halogen gases cause significant cardiac injury, dysfunction, and failure that can be critical in causing mortalities following exposures. Our studies also demonstrated that cardiac dysfunction occurs as a result of a direct insult independent of coexisting hypoxia, since it is not fully reversed by oxygen supplementation. Therefore, studies on offsite organ effects of inhaled toxic gases can impact development of treatment strategies upon accidental or deliberate exposures to these agents. Here we summarize the knowledge of cardiovascular effects of common inhaled toxic gases with the intent to highlight the importance of consideration of cardiac symptoms while treating the victims.
      PubDate: 2015-09-22
      DOI: 10.14800/crm.997
      Issue No: Vol. 1 (2015)
       
  • H2S epigenetic regulation of vascular cell functions

    • Authors: Guangdong Yang
      Abstract:     The physiological and biomedical importance of H2S in cardiovascular system has been extensively studied, and H2S is involved the regulation of vascular tone, angiogenesis, cell growth and differentiation, inflammation, and energy generation, etc. In blood vessels, cystathionine gamma-lyase (CSE) seems to be the major H2S-producing gene expressed in both smooth muscle and endothelium. Abnormal metabolism and functions of the CSE/H2S pathway have been linked to various cardiovascular diseases, including atherosclerosis and hypertension. It is known now that H2S posttranslationally modification of proteins by S-sulfhydration contributes to the major bioactivities of H2S. Cardiovascular disorders and epigenetics are closely associated, and epigenetics has become a promising field in cardiovascular research. In this research highlight, I discuss the latest published findings on H2S signalling in epigenetic regulation of vascular cell functions via modification of DNA methylation and DNA damage repair.
      PubDate: 2015-09-02
      DOI: 10.14800/crm.967
      Issue No: Vol. 1 (2015)
       
  • Transthyretin amyloidosis: an over review

    • Authors: Alina Tantau, Mihaela Laszlo, Istvan Laszlo
      Abstract: Amyloidosis refers to the extracellular deposition of fibrils that are composed of low molecular weight subunits of a variety of serum proteins. The most common familial amyloidosis is caused by the transthyretin protein. People who are born with inherited mutations in the transthyretin gene produce abnormal, (“variant”) transthyretin throughout their liver.The clinical manifestations vary, depending upon the particular substitution, but result either in neuropathy, cardiomyopathy, or both.One of the most common hereditary transthyretin amyloid cardiomyopathies is caused by the Val122IIe mutation. Progressive amyloid deposition in the myocardium and/or in the electrical conduction system is responsible for restrictive cardiomyopathy and unpredictable episodes of arrhythmias and/or severe conduction disorders.The vast majority of transthyretin-familial amyloidotic polyneuropathy cases are associated with Val30Met mutation. The main neuropathic feature of transthyretin amyiloidosis is a progressive sensorimotor and autonomic neuropathy.The first step in evaluating a patient with transthyretin amyloidosis consists in establishing the diagnosis and then evaluating the extent of disease. Deposition of amyloid via tissue can be demonstrated by Congo red staining of biopsy specimens. In all cases, amyloid typing has to be completed by transthyretin gene sequencing and by immunofixation electrophoresis of serum and urine.Current treatment options for patients with transthyretin amyiloidosis are limited. For patients with transthyretin-primary familial amyloidosis who have mild or moderate disease and a diagnosis confirmed by genetic testing and biopsy, liver transplant is the current standard of care.
      PubDate: 2015-08-25
      DOI: 10.14800/crm.952
      Issue No: Vol. 1 (2015)
       
  • MicroRNAs as solutions are producing big power for heart regeneration

    • Authors: Yanhan Dong, Yanyan Yang, Kun Wang, Jianxun Wang, Peifeng Li
      Abstract: Cardiovascular diseases have become a predominant cause of mankind death globally. In order to overcome the limited capacity of adult mammalian heart to regenerate for cardiac injury, promising progress has been made in uncovering molecular mechanisms that will promote cardiac regeneration. Recently, small non-coding RNAs, known as microRNAs (miRNAs) that alter target expression by post-transcriptional regulation of gene expression, have been demonstrated essential to cardiac development, pathology, regeneration and repair. These observations imply that miRNAs are potential therapeutic targets for patients with congenital and acquired cardiovascular diseases. In this review, we discuss the current findings attesting to the critical roles of miRNAs in heart morphogenesis, and the possibility of employing miRNAs to change cells fate and enhance cardiac regeneration. 
      PubDate: 2015-08-17
      DOI: 10.14800/crm.947
      Issue No: Vol. 1 (2015)
       
  • Intrinsic nanomechanical changes in live diabetic cardiomyocytes

    • Authors: Juan Claudio Benech, Nicolás Benech, Ana I. Zambrana, Inés Rauschert, Verónica Bervejillo, Natalia Oddone, Andrés Alberro, Juan P. Damián
      Abstract: Patients with diabetes develop a cardiomyopathy that is independent of both coronary artery disease and hypertension and contributes to mortality and morbidity caused by diabetes. The mechanisms underlying the development of diabetic cardiomyopathy are poorly understood. Increased diastolic left ventricular (LV) stiffness is an early manifestation of diabetic myocardial dysfunction. This increase is usually attributed to myocardial fibrosis or to myocardial deposition of advanced glycation end products. Alteration of the stiffness (resting tension) of the diabetic cardiomyocyte was also proposed to be an important factor contributing to increased LV stiffness. Some of these data were obtained from isolated cardiomyocytes from human frozen biopsy samples that had been thawed, mechanically disrupted, and incubated with Triton X-100, disrupting sarcolemmal and sarcoplasmic membranes. We therefore determined the stiffness of live isolated cardiomyocytes from control and streptozotocin-treated mice using atomic force microscopy (AFM) nanoindentation. We show that 3 months of type 1 diabetes provoked fragmentation and disorder of myocardial fibers, interstitial collagen deposition, reduction in SERCA2a calcium pump expression and changes in F-actin organization. Moreover, we show that live isolated diabetic cardiomyocytes are stiffer than control cardiomyocytes when tested in Tyrode buffer with different ionic compositions. Hence, it is very likely that intrinsic mechanical changes of cardiomyocytes are an important factor in increasing myocardial stiffness in vivo.
      PubDate: 2015-08-03
      DOI: 10.14800/crm.893
      Issue No: Vol. 1 (2015)
       
  • LINKING CARDIAC INSULIN RESISTANCE AND HEART FAILURE: GRK2 AS AN
           INTEGRATIVE NODE.

    • Authors: Elisa Lucas, Maria Jurado-Pueyo, Rocio Vila-Bedmar, Javier Diez, Federico Mayor Jr., Cristina Murga
      Abstract: G protein-coupled receptor kinase 2 (GRK2) has arisen as a signaling hub with critical regulatory roles in cardiac function and dysfunction. Cardiac GRK2 levels are increased during hypertension, cardiac ischemia and heart failure both in humans and in experimental models, whereas genetic inhibition of GRK2 is cardioprotective in different animal models of these pathologies. However, the mechanistic basis of these effects is not fully understood. Recent recent research has indicated that GRK2 not only phosphorylates and desensitizes G protein-coupled receptors (GPCR) that are important for heart function such as β-adrenergic or angiotensin type 1, but also modulates other pathways relevant for cardiac physiology such as the insulin signaling cascade. Using GRK2 hemizygous (GRK2+/-) mice, we have unveiled that a lower GRK2 dosage promotes enhanced insulin sensitivity in adult murine hearts what correlates with a cardioprotective gene expression profile. Also, GRK2 levels increase in cardiac tissue in well-established experimental models of systemic insulin resistance, such as high fat diet (HFD) feeding or ob/ob mice what parallels the impaired cardiac insulin sensitivity observed in these conditions. Our findings suggest that pathological inputs of different etiology such as increased catecholamine levels or high dietary fat converge in common important nodes key to the progress of the pathology. One such key connecting hub is GRK2, whose enhanced cardiac expression would promote progression towards maladaptive myocardial remodeling and heart failure.
      PubDate: 2015-02-09
      DOI: 10.14800/crm.586
      Issue No: Vol. 1 (2015)
       
  • MicroRNAs Inducing Proliferation of Quiescent Adult Cardiomyocytes

    • Authors: Raghav Pandey, Rafeeq PH Ahmed
      Abstract: In the United States, each year over 700,000 people suffer from a heart attack and over 25% of deaths are related to heart disease, making it the leading cause of death. Following ischemic injury a part of the heart muscle is replaced by a scar tissue, reducing its functioning capacity. Recent advancements in surgical intervention and pharmacotherapy only provide symptomatic relief without addressing the root cause of the problem which is the massive loss of cardiomyocytes (CM). Therefore, the development of novel curative intervention for myocardial repair and regeneration remains an area of intense research. While existing CM in zebra fish and neonatal mice are known to proliferate and replenish the infarcted heart, it has been shown that adult mammalian CM lose this ability, thus preventing regeneration of the scar tissue. There have been many attempts to facilitate regeneration of ischemic heart but have met with limited success. Micro-RNAs (miRNAs) are one of the promising candidates towards this goal as they are known to play important regulatory roles during differentiation and tissue regeneration, and regulate genetic information by post-transcriptional modification as well as regulation of other miRNAs. While previous work by Eulalio et al., showed miRNAs inducing proliferation in neonatal CM (NCM), we here identify miRNAs inducing proliferation of rat adult-CM (ACM). This commentary while analyses recent work by Eulalio et al also shows some new data with microRNAs in rat adult-CMs. Further work into the mechanism of these miRNAs can determine their therapeutic potential towards regenerating cardiac tissue post ischemic injury.   
      PubDate: 2015-01-28
      DOI: 10.14800/crm.519
      Issue No: Vol. 1 (2015)
       
  • Crosstalk between Src and β-arrestin2 orchestrates cardiac hypertrophic
           responses under mechanical stresses

    • Authors: Shijun Wang, Jian Wu, Zhen Wang, Yunzeng Zou
      Abstract: The activity of Src, one of the non-receptor tyrosine kinase family proteins, is increased during mechanical stretch-evoked cardiac hypertrophy. Angiotensin II (AngII) type 1 receptor (AT1-R) plays a pivotal role in hypertrophic responses under mechanical stresses independently of Ang II. However, whether Src is critically involved in AngII-independent AT1-R signaling transduction and cardiac hypertrophy is not yet clear. Here we have reported that Src tyrosine kinase is activated and recruited by β-arrestin2, both bind to membrane AT1-R and trigger the intracellular ERK1/2 signaling pathway, leading to the development of cardiac hypertrophy. Our findings highlight that mechanical stretch-induced, β-arrestin2-dependent Src-ERK hypertrophic pathway, might be partly different from the Ang-II-induced one, which is dependent on G protein coupling. In the former, neither Gαq-mediated protein kinase C (PKC) nor IP3 are activated by mechanical stretch in cardiomyocytes, however, inhibition of Src kinase causes attenuation of ERK1/2 signaling and improves pressure overload-induced cardiac hypertrophy and dysfunction in mice lacking AngII. Our work suggests that Src might be one of the potential therapeutic targets for pressure overload-induced myocardial remodeling.
      PubDate: 2015-01-03
      DOI: 10.14800/crm.484
      Issue No: Vol. 1 (2015)
       
 
 
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