The possibility of regeneration of cardiac muscle tissue. Muscle tissue epidermal and neural origin

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Описание работы

1. The absence of stem cells in cardiac muscle tissue, the inability to regenerate cardiomyocytes.
2. Features of age-related changes in the smooth muscle tissue, cardiac muscle tissue and in skeletal muscle tissue.

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The possibility of regeneration of cardiac muscle tissue. Muscle tissue epidermal and neural origin.


The purpose:

  1. Know muscle as the body.
  2. To know the microscopic structure of cardiac muscle tissue..
  3. Know the structural features of the two types of functions of cardiac muscle tissue.


1. The absence of stem cells in cardiac muscle tissue, the inability to regenerate cardiomyocytes. 
2. Features of age-related changes in the smooth muscle tissue, cardiac muscle tissue and in skeletal muscle tissue.

































Muscle tissue is composed of differentiated cells contractile proteins. The structural biology of

these proteins generate the forces necessary for cellular contraction which drives movement

within certain organs and the body as a whole. Most muscle cells are of mesodermal origin, and

they are differentiated mainly by a gradual process of lengthening, which simultaneous synthesis

of myofibrillar proteins.

Three types of muscle tissue in mammals can be distinguished on the basis of morphologic and

functional characteristics, and each type of muscle tissue has a structure adapted to its

physiologic role.

Cardiac muscle (heart muscle) is involuntary striated muscle that is found in the walls and histological foundation of the heart, specifically the myocardium. Cardiac muscle is one of three major types of muscle, the others being skeletal and smooth muscle. These three types of muscle all form in the process of myogenesis. The cells that constitute cardiac muscle, called cardiomyocytesor myocardiocytes, contain only three nuclei.[1][2][page needed] The myocardium is the muscle tissue of the heart, and forms a thick middle layer between the outer epicardium layer and the inner endocardium layer.

Coordinated contractions of cardiac muscle cells in the heart propel blood out of the atria and ventricles to the blood vessels of the left/body/systemic and right/lungs/pulmonary circulatory systems. This complex mechanism illustrates systole of the heart.

Cardiac muscle cells, unlike most other tissues in the body, rely on an available blood and electrical supply to deliver oxygen and nutrients and remove waste products such as carbon dioxide. The coronary arteries help fulfill this function.





The three types of adult muscle have different potentials for regeneration after injury.

1. Cardiac Muscle – has virtually no regenerative capacity beyond early childhood. Defects

or damages (e.g. Infarcts) in heart muscle are generally replaced by the proliferation of

connective tissue, forming myocardial scars.

2. Skeletal Muscle – the nuclei are incapable of undergoing mitosis, the tissue can undergo

limited regeneration. The source of regenerating cells is believed to be the satellite cells.

3. Smooth Muscle – is capable of an active regenerative response. After injury, viable

mononucleated smooth muscle cells and pericytes from blood vessels undergo mitosis

and provide for the replacement of the damaged tissue.




















1. The absence of stem cells in cardiac muscle tissue, the inability to regenerate cardiomyocytes. 

In biology, regeneration is the process of renewal, restoration, and growth that makes genomes, cells, organisms, andecosystems resilient to natural fluctuations or events that cause disturbance or damage. Every species is capable of regeneration, from bacteria to humans.[1][2] Regeneration can either be complete[3] where the new tissue is the same as the lost tissue,[3] or incomplete[4] where after the necrotic tissue comes fibrosis.[4] At its most elementary level, regeneration is mediated by the molecular processes of gene regulation.[5][6] Regeneration in biology, however, mainly refers to themorphogenic processes that characterize the phenotypic plasticity of traits allowing multi-cellular organisms to repair and maintain the integrity of their physiological and morphological states. Above the genetic level, regeneration is fundamentally regulated by asexual cellular processes.[7] Regeneration is different from reproduction. For example, hydra perform regeneration but reproduce by the method of budding.

The hydra and the planarian flatworm have long served as model organisms for their highly adaptive regenerative capabilities.[8] Once wounded, their cells become activated and start to remodel tissues and organs back to the pre-existing state.[9] The Caudata ("urodeles"; salamanders and newts), an order of tailed amphibians, is possibly the most adeptvertebrate group at regeneration, given their capability of regenerating limbs, tails, jaws, eyes and a variety of internal structures.[1] The regeneration of organs is a common and widespread adaptive capability among metazoan creatures.[8] In a related context, some animals are able to reproduce asexually through fragmentation, budding, or fission.[7] A planarian parent, for example, will constrict, split in the middle, and each half generates a new end to form two clones of the original.[10]Echinoderms (such as the starfish), crayfish, many reptiles, and amphibians exhibit remarkable examples of tissue regeneration. The case of autotomy, for example, serves as a defensive function as the animal detaches a limb or tail to avoid capture. After the limb or tail has been autotomized, cells move into action and the tissues will regenerate.[11][12][13]Ecosystems are regenerative as well. Following a disturbance, such as a fire or pest outbreak in a forest, pioneering specieswill occupy, compete for space, and establish themselves in the newly opened habitat. The new growth of seedlings andcommunity assembly process is known as regeneration in ecology.

Regeneration of heart muscle cells

Until recently, it was commonly believed that cardiac muscle cells could not be regenerated. However, a study reported in the April 3, 2009 issue of Science contradicts that belief.[10] Olaf Bergmann and his colleagues at the Karolinska Institute in Stockholm tested samples of heart muscle from people born before 1955 had very little cardiac muscle around their heart, many showing with disabilities from this abnormality. By using DNA samples from many hearts, the researchers estimated that a 20-year-old renews about 1% of heart muscle cells per year, and about 45 percent of the heart muscle cells of a 50-year-old were generated after he or she was born.

One way that cardiomyocyte regeneration occurs is through the division of pre-existing cardiomyocytes during the normal ageing process.[11] The division process of pre-existing cardiomyocytes has also been shown to increase in areas adjacent to sites of myocardial injury. In addition, certain growth factors promote the self-renewal of endogenous cardiomyocytes and cardiac stem cells. For example, insulin-like growth factor 1, hepatocyte growth factor, and high-mobility group protein B1 increase cardiac stem cell migration to the affected area, as well as the proliferation and survival of these cells.[12] Some members of the fibroblast growth factorfamily also induce cell-cycle re-entry of small cardiomyocytes. Vascular endothelial growth factor also plays an important role in the recruitment of native cardiac cells to an infarct site in addition to its angiogenic effect.

Based on the natural role of stem cells in cardiomyocyte regeneration, researchers and clinicians are increasingly interested in using these cells to induce regeneration of damaged tissue. Various stem cell lineages have been shown to be able to differentiate into cardiomyocytes, including bone marrow stem cells. For example, in one study, researchers transplanted bone marrow cells, which included a population of stem cells, adjacent to an infarct site in a mouse model. Nine days after surgery, the researchers found a new band of regenerating myocardium.[13] However, this regeneration was not observed when the injected population of cells was devoid of stem cells, which strongly suggests that it was the stem cell population that contributed to the myocardium regeneration. Other clinical trials have shown that autologous bone marrow cell transplants delivered via the infarct-related artery decreases the infarct area compared to patients not given the cell therapy.

Dog cardiac muscle (400X)



Cardiac muscle is striated, like skeletal muscle, as the actin and myosin are arranged in sarcomeres, just as in skeletal muscle.

However, cardiac muscle is involuntary.

Cardiac muscle cells usually have a single (central) nucleus. The cells are often branched, and are tightly connected by specialised junctions. The region where the ends of the cells are connected to another cell is called an intercalated disc.

The intercalated disc contains gap junctions, adhering junctions and desmosomes.

Gap junctions allow the muscle cells to be electrically coupled, so that they beat in synchrony.


Cardiac muscle (heart muscle), like skeletal muscle, is also striated but involuntary muscle

responsible for the pumping activity of the vertebrate heart. The individual muscle cells are

joined through a junctional complex known as the intercalated disc and are not fused together

into multinucleate structures as they are in skeletal muscle.

Though unlike skeletal, cardiac muscle cells are short and branched with a single, centered

nucleus. They are also involuntary or not under immediate conscious control. Rather than Z-disks, which join skeletal muscle cells, intercalated disks join cardiac muscle fibers.

Cardiac muscles are located only in the heart. Unlike skeletal, cardiac muscle can contract

without extrinsic nerve or hormonal stimulation. It contracts via its own specialized conducting

network within the heart, with nerve stimulation causing only an increase or decrease in rate of

conducting discharge. The heart also has some very beneficial features such as an increased

number and larger mitochondria, which allow it to produce more ATP. This is very important

since the heart is constantly contracting and relaxing. Cardiac muscle can also convert lactic acid produced by skeletal muscle to ATP. This is quite ingenious since lactic acid is a by-product of muscle when in a deoxygenated state, a state that would be detrimental to cardiac muscle. This muscle also remains contracted 10 to 15 times longer than skeletal muscle due to a prolonged delivery of calcium (see discussion of cardiac action potential in Circulation section). Likewise, it also has a relatively long refractory period, lasting several tenths of a second, allowing heart to relax between beats. This also allows heart rate to increase significantly without causing it to go into tetanus, which would be fatal since it would cause blood flow to cease.





































Several animals can regenerate heart damage, but in mammals cardiomyocytes (heart muscle cells) cannot proliferate (multiply) and heart damage causes scarring and fibrosis. The long held view was that mammalian cardiomyocytes are terminally differentiated and cannot divide. However inhibition of p38 MAP kinase was found to induce mitosis in adult mammalian cardiomyocytes.[51] Treatment with FGF1 and p38 MAP kinase inhibitors regenerates the heart, reduces scarring, and improves cardiac function in rats with cardiac injury.

Clinical significance[edit]

Occlusion (blockage) of the coronary arteries by atherosclerosis and/or thrombosis can lead to myocardial infarction (heart attack), where part of the myocardium is injured due toischemia (not receiving enough oxygen). Certain viruses lead to myocarditis (inflammation of the myocardium). Cardiomyopathies are inherent diseases of the myocardium, many of which are caused by genetic mutations.





















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