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p> Background: Aging of the myocardium is a dynamic process which involves progressive loss of cardiomyocytes due to necrosis and apoptosis, interstitial fibrosis and reactive hypertrophy of the remaining vital cardiomyocytes. In our study, we investigated the postnatal changes in the myocardium of 15 adult male Wistar rats, distributed in the foll...
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Aim:
Circulating microRNA expression has become a biomarker of cardiovascular disease; however, the association of microRNA expression between circulation and myocardium in hypertrophic cardiomyopathy remains unclear. This study aimed to find a circulating biomarker correlated not only to myocardial expression, but also to cardiac hypertrophy and...
Citations
... We chose the heart as a model due to its high metabolic activity as well as its great clinical significance related to aging (Strait and Lakatta 2012). The aging heart is characterized by progressive reactive interstitial fibrosis and hypertrophy in both ventricles (Biernacka and Frangogiannis 2011;Kotov et al. 2017). We reported earlier that aging in both ventricles was characterized by hypertrophy of cardiomyocytes and increased accumulation of complex collagen deposits in the interstitial space and perivascular zone. ...
... We reported earlier that aging in both ventricles was characterized by hypertrophy of cardiomyocytes and increased accumulation of complex collagen deposits in the interstitial space and perivascular zone. These changes were more prominent in the LV than in the RV due to the higher afterload (Kotov et al. 2017). Prominent fibrotic changes also are evident in the RV with advancing age (Kotov et al. 2017). ...
... These changes were more prominent in the LV than in the RV due to the higher afterload (Kotov et al. 2017). Prominent fibrotic changes also are evident in the RV with advancing age (Kotov et al. 2017). Fibroblasts are important participants in the development of fibrosis; they can transform into the myofibroblast phenotype and promote myofibroblast-promoted collagen turnover (Biernacka and Frangogiannis 2011). ...
Age-related morphological and physiological changes occur in cells, tissues and organs with high metabolic or mitotic activity; these changes decrease their regenerative capacity. One such change is interstitial fibrosis. Mast cells contain basic fibroblast growth factor and have been related to pro-fibrotic activity. We investigated the role of mast cells in physiological aging of the heart and kidney. We analyzed changes in mast cell number and compared the left and right heart ventricles and kidneys of 6- and 12-month-old Wistar rats. We also evaluated the immunohistochemical expression of basic fibroblast growth factor. Finally, we analyzed changes in the extent of interstitial fibrosis and in the glomerular sclerosis index as nonspecific markers of aging and correlated these parameters with of mast cells. Mast cells were visualized by toluidine blue staining and specific immunohistochemical expression of tryptase. The expression of basic fibroblast growth factor was assessed semiquantitatively. The extent of interstitial fibrosis was investigated using Mallory's trichrome staining. Glomerular sclerosis was evaluated using periodic acid-Schiff staining. We found that the number of mast cells increased significantly in the older rats. We also found that the number of mast cells was greatest in the left ventricle followed by the right ventricle, then the kidney. The immunoreactivity of basic fibroblast growth factor also increased in older animals. Correlations between the number of mast cells and immunoreactivity of basic fibroblast growth factor, extent of interstitial fibrosis and glomerular sclerosis index demonstrated the association between mast cells and age-related tissue remodeling of the heart and kidney.
... 23 For this reason, the ratio between aged and young cardiomyocytes, together with the total number of cardiomyocytes can be used as a prognostic marker of the ability of the myocardium to preserve or worsen its function. 24 In support of this, our previous studies [25][26][27][28] have shown that aging of the myocardium is characterised by an increase in the amount of collagen, a decrease in capillary density and changes in the activity of enzymes of the NOS group, which may explain the onset of dysfunction in the aging myocardium. These data and the results of the present study, in line with evidence from the relevant literature lead to the conclusion that as aging advances, the morphology and the structure of the heart become impaired both at the level of the organ and at the level of the individual cardiomyocyte. ...
Background: The growth of the heart during the foetal and early postnatal development takes places mainly due to hyperplasia. The late postnatal development is characterised by cardiomyocytic hypertrophy in response to normal physiological mechanisms and increased load. To study the cell size most authors measure the diameter either directly or indirectly.
Aim: The aim of the present study was to make a comparative quantitative analysis of the postnatal changes observed in the left and right ventricles in rat by evaluating the changes in three morphometric parameters – thickness of the free wall, transverse section of the cardiomyocytes and cardiomyocytic density in the left ventricle and right ventricle.
Materials and methods: In the present study, we used histological material from the hearts of 15 male Wistar rats, distributed in fi ve groups aged 2 weeks, 1 month, 3 months, 6 months and 12 months, respectively.
Results: In both ventricles, the wall thickness and the transverse section of the cardiomyocytes increased with age, while the cardiomyocytic density decreased. Changes were identical in both ventricles; however, they were more dynamic and pronounced in the left ventricle.
Conclusions: The studied morphometric parameters reveal that age-related hypertrophy and the gradual loss of cardiac muscle cells take place in both ventricles but have a more dynamic pattern of progression in the left ventricle as compared with the right ventricle.
... These changes in the parameters may be interpreted as a compensatory response of the myocardium at the cellular level, intended to decrease the effects of increased pre-and afterload of the heart [2]. Our previous studies have shown that the myocardial response to increased stress includes ventricular remodelling with accumulation of collagen and development of reactive fibrosis [21], a specific location-targeted up-regulation of enzymes of the NOS group [13][14][15] and a decrease in the capillary density [16]. ...
... Moreover, the hypertrophied myocardium contained zones of replacement fibrosis in the place of cardiomyocytes which had undergone atrophic deformations and/or loss [24]. The presence of such replacement fibrosis has been confirmed by our previous studies [21]. These changes in the normal architectonics of the myocardium may predispose it towards development of arrhythmias due to the discontinuous conduction [24]. ...
Background:
Differences in the size of cardiac muscle cells observed in normal and hypertrophic hearts have been assessed through different methodologies. Spontaneously hypertensive rats are often used as an experimental model of essential hypertension in humans, which allows researchers to study the relation between hypertension and cardiac hypertrophy. It has been shown that ventricular hypertrophy in mammals progresses and ventricular failure develops in the end stage of hypertrophy. The aim of the present study was to analyse a number of morphometric markers and compare them between male normotensive Wistar rats and male spontaneously hypertensive rats.
Materials and methods:
The total number of male Wistar rats was 15, distributed in five age groups, each containing three animals: two-weeks-old; one-month-old; three-months-old; six-months-old; twelve-months old. The male spontaneously hypertensive rats were distributed in two age groups, each containing three animals: one-month-old (young) and six-months-old (adult) RESULTS: As aging progressed, both in male normotensive Wistar rats and in male spontaneously hypertensive rats we noted a statistically significant increase in the morphometric parameters thickness of the free wall and the cross-sectional area of the cardiomyocytes and their nuclei and a decrease in the cardiomyocytic density in both ventricles. These changes were more pronounced and occurred at an earlier age in spontaneously hypertensive rats.
Conclusions:
The present study analyses in detail the alterations in the myocardium of the left and right ventricle, initiated by age-related hypertrophy, as well as hypertrophy induced by arterial hypertension.
... The change in the quantity of the collagen fibres of the connective tissue is the most significant marker of physiological processes such as aging of the myocardium, as well as pathological conditions associated with increased load and impaired function of the heart. [20][21][22][23] The intercalated disc is the zone of contact between the adjacent cardiomyocytes in longitudinal direction. It consists of two parts: transversal part and lateral part. ...
... In addition, some of the cytoskeleton's components take part in other cell processes such as hypertrophy, cell division, migration, intracellular vesicular transport, arrangement and function of cellular components, disposition of membrane receptors and intercellular communication. [8][9][10][21][22][23] It is suggested that the cytoskeleton plays a key role in the mechanical signal transduction of the cell. [33] For an easier examination and understanding of its function, the cytoskeleton is divided, based on its morphology and topography, into different types: sarcomeric, extrasarcomeric, membrane-submembrane, nuclear. ...
Many questions regarding the morphology of the cardiovascular system are yet to be answered. In particular, elucidating the core principles of the architectonics of the myocardium is of great importance for the understanding of the exact mechanisms of the cardiac functions and the pathogenic processes which constitute a prerequisite for cardiovascular diseases. A number of contemporary studies reveal the importance of the myocardium in almost every disease – either as a primary pathophysiological unit or as the target of the pathological damage. It has to be stated that the myocardium has a remarkable diagnostic and therapeutic potential. It is comprised of various types of cells – contractile cardiomyocytes of the atria and ventricles, cells of the sinoatrial node and Purkinje fibres, the latter two being part of the conducting system of the heart. The ultrastructural components of these cells include the various structures which ensure cellular contact and communication, the specialised structures of the cellular and the sarcoplasmic membrane and the different elements of the complex cytoskeleton. Furthermore, the orientation of the cardiomyocytes plays a key role not only for the mechanical contraction but also in the electric conduction and the energy metabolism of the cardiac muscle. Studies on the size, alignment and specific characteristics of the cardiomyocytes have the potential to provide a morphological base for the diagnostics of various cardiac pathologies.
The present chapter attempts a detailed yet comprehensive account of the exceedingly complex molecular events involved in heart development, including description of the main differentiation signaling pathways, transcription factors, enhancers and gene regulatory networks, with a special emphasis on applying this continuously enlarging body of modern scientific knowledge to the field of stem cell differentiation into cardiomyocytes for diagnostic and therapeutic applications. MicroRNAs are also emerging as an important area of discovery aiming to revolutionize current therapies in cardiology, therefore we describe their involvement in cardiogenesis, proliferation/apoptosis, angiogenesis, fibrosis and hypertrophy. After reviewing the architectural organization, ultrastructure details and functional compartments of cardiomyocytes derived from in vitro and in vivo studies, we focus on molecular mechanisms involved in cardiac hypertrophy and fibrosis, particularly on calcium signaling events triggering these excessive adaptive responses. Further, we stress the embryogenetic and molecular differences between the right and left ventricle, as well as their pathophysiology specificities and clinical consequences.
Introduction: Spontaneously hypertensive rats are often used as a
model of arterial hypertension in humans. Cardiomyocytic hypertrophy, focal
myocytolysis and ventricular fibrosis are only a part of the alterations in the
morphology of the myocardium observed in spontaneously hypertensive rats
with the progression of hypertension. The present manuscript reviews our
studies on spontaneously hypertensive rats, with focus on the microscopic
changes in the myocardial architectonics and analysis of several morphometric
parameters.
Materials and methods: A total of 12 male spontaneously hypertensive
rats, distributed in two age groups, each containing six animals: 1-monthold
(young) and 6-months-old (adult) were used. We also used 12 male
normotensive Wistar rats, distributed in two age groups, each containing six
animals: 1-month-old (young) and 6-months-old (adult). Routine haematoxylin
and eosin staining and Mallory’s trichrome stain were conducted. Quantitative
data were obtained with a computerized system for image analysis NISElements
Advanced Research (Ver. 2.30).
Results: Changes in the normal morphology of the myocardium included
cardiomyocytic hypertrophy, focal myocytolysis and ventricular fibrosis. As
aging progressed, we noted a significant increase in the thickness of the free
wall and cross-sectional area of the cardiomyocytes and the cardiomyocytic
nuclei and a decrease in cardiomyocytic density.
Conclusion: The manuscript presents a detailed qualitative and quantitative
study of changes in the normal structure of the myocardium initiated by
arterial hypertension.
