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Vooruitgang in de regeneratie van beschadigd hart

Recente tweelingstudies hebben nieuwe manieren aangetoond om een ​​beschadigd hart te regenereren

Heart failure affects at least 26 million people worldwide and is responsible for numerous fatal deaths. Due to rise in ageing population, taking care of the hart- is becoming a need leading to rise in expenditures. There have been significant advances in therapeutic treatments for the hart- en er worden veel preventieve maatregelen genomen, maar de mortaliteit en morbiditeit zijn nog steeds erg hoog. Er zijn zeer weinig behandelingsopties beschikbaar en meestal berust het op harttransplantatie voor de patiënten die zich echt in het eindstadium bevinden en op weg zijn naar volledig hartfalen.

Our body does have an extraordinary capacity to heal itself, for example liver can be regenerated when is damaged, our skin also most of time and one kidney could take over the function for two. Unfortunately, this is not true for most of our vital organs – including the heart. When a human heart is damaged – caused by a disease or an injury – the damage is perpetual. Example, after a heart attack, millions or billions of heart muscle cells can be lost forever. This loss weakens the heart gradually and leads to serious conditions like heart failure, or scars in the heart which can prove fatal. Heart failure usually results when cardiomyocytes (type of cells) become deficient. Unlike newts and salamanders, human adults cannot spontaneously regrow damaged organs such as the heart. In a human embryo or when a baby is growing in the womb, hart- cells divide and multiply which helps the heart to grow and develop for nine months. But mammals including humans do not possess the ability to regenerate the heart as they lose this ability subsequently and completely after about a week of being born. Heart muscle cells lose their ability to divide and multiply and hence cannot regenerate. This is true for other human cells too – brain, spinal cord enz. Aangezien deze volwassen cellen zich niet kunnen delen, kan het menselijk lichaam de beschadigde of verloren gegane cellen niet vervangen en dit leidt tot ziekten. Hoewel dit ook de reden is waarom er nooit een harttumor is, worden tumoren veroorzaakt door ongecontroleerde groei van cellen. Als het echter mogelijk wordt gemaakt dat deze cellen zich weer gaan delen, kan dit leiden tot 'regeneratie' van een aantal weefsels en helpen bij het herstel van een orgaan.

De enige optie die iemand heeft als hij lijdt aan een zwakke of beschadigd hart or a heart disease is to receive a heart transplant. This has multitude of aspects which generally affect a transplant from becoming a reality in most patients. Firstly, the heart that is donated by a “donor” has to be a healthy heart before the donor passed away, which means that the heart needs be harvested from young people who have died because of illness or injuries and these conditions have not affected their hart- in any way. The prospective recipient patient must match with the donor heart to receive the transplant. This translates into a long wait. As a possible alternative, the potential to be able to create new muscle in the heart through cell division could offer hope to millions with damaged heart. Many procedures have been tried and tested by the scientific community, however, results so far have been ineffective.

In een nieuwe studie gepubliceerd in Cel, onderzoekers van de Universiteit van Californië, San Francisco, VS hebben voor het eerst een efficiënte en stabiele methode in diermodellen ontwikkeld om volwassen hartcellen (cardiomyocyten) te laten delen en zo mogelijk het beschadigde deel van het hart te herstellen1. The authors identified four genes which are involved in cell division (that is cells which multiply on their own). When these genes were combined with genes which cause mature cardiomyocytes to re-enter into a cell cycle, they saw that cells were dividing and reproducing. So, when the function of these four essential genes was enhanced, the hart- tissue showed regeneration. After heart failure in a patient, this combination improves heart function. Cardiomyocytes exhibited 15-20 percent division in the current study (compared to 1 percent in earlier studies) cementing reliability and efficiency of this study. This study could technically be extended tp other organs because these four genes are a common feature. This is a very relevant work because any study on the hart- is firstly very complicated and secondly the delivery of genes has to be done with caution so as not to cause any tumours in the body. This work could turn into a very powerful approach for regenerating the heart and also other organs.

Another study by Stem Cell Institute, University of Cambridge, UK, has developed an innovative way to repair hart- tissue such that a donor would not be required at all2. They have used stem cells to grow live patches of “heart muscle” in the laboratory which are only 2.5 square centimetres but they look like a powerful potential tool to treat patients who have heart failure. These patches have a bright prospective of getting naturally assimilated into a patient’s hart- i.e. it’s a “fully functional” tissue which beats and contracts just like a normal heart muscle. An earlier approach of injecting stem cells into the body to repair the heart has been unsuccessful because stem cells did not stay in the hart- muscle but instead got lost in the blood. The current patch is a “live” and “beating” heart tissue that can be attached to an organ (in this case the hart-) and thus any damage could be repaired. Such patches could be grown as and when there is a demand for a patient. This would essentially surpass the need to wait for a matching donor. These patches could also be grown using the hart- patient’s own cells eliminating the risks that are involved in organ transplant. Assimilating the patch into a beschadigd hart is an invasive procedure and requires correct electrical impulses for making the hart- beat well-integrated with a patch. But the risks involved in this kind of procedure are better that a total heart transplant which is much more invasive. The team is getting ready for animal trials and clinical trials within 5 years before this could be used widely for hart- patiënten.

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{U kunt de originele onderzoekspaper lezen door op de DOI-link hieronder in de lijst met geciteerde bron(nen) te klikken}

Bron (nen)

1. Mohamed et al. 2018,. Regulering van de celcyclus om de proliferatie van volwassen cardiomyocyten en hartregeneratie te stimuleren. Celhttps://doi.org/10.1016/j.cell.2018.02.014

2. Universiteit van Cambridge 2018. Een gebroken hart oplappen. http://www.cam.ac.uk/research/features/patching-up-a-broken-heart. [Toegang tot 1 mei 2018]

SCIEU-team
SCIEU-teamhttps://www.ScientificEuropean.co.uk
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