Slowing down and stopping the process of tissue regeneration due to impaired cell division leads to aging.
Scientists from the Spanish National Cancer Centre (CNIO) have concluded that the severity of coronavirus infection depends on the length of telomeres – the “tips” of DNA that protect chromosomes from damage.
According to scientists, one of the consequences of a viral infection is the shortening of telomeres, which, in turn, interferes with the regeneration of lung tissue and causes longer-term complications in some patients.
“Usually telomere length decreases with aging, but in the case of severe forms of COVID-19, this trend has been observed regardless of the person’s age. The study found that telomeres were significantly shorter in those people who suffered from COVID-19 in the most severe form. At the same time, the age of the sick did not affect this pattern in any way,” the study says.
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Scientists usually associate telomere length with aging, because each time a cell divides, telomeres are shortened and gradually the cell is damaged and stops dividing. As a result, impaired cell division leads to aging.
“The new findings are consistent with earlier studies showing that one of the causes of pulmonary fibrosis (including those characteristics of COVID-19) is damage to the telomeres of cells involved in lung tissue regeneration. These cells are called type II pneumocytes and it is them that SARS-CoV-2 uses to infect in the lungs,” experts say.
Scientists have previously demonstrated that experimental therapy for telomere lengthening by activating the enzyme telomerase has a therapeutic effect on lung fibrosis and other diseases associated with telomeres shortening. They now hope to test the approach for COVID-19 as well.