Coronavirus Úrscéal: Cén Fáth a Mharaíonn an Corónach Daoine Scothaosta? Nádúr: Víris Scamhóga Aois

Dec 22, 2021

Léiríonn sonraí údarásacha go bhfuil meánaois na mbásanna COVID-19 ar fud an domhain os cionn 70 bliain!


Cén fáth go bhfuil níos mó seans ann go bhfaighidh daoine scothaosta bás de bharr ionfhabhtuithe nua-coronavirus ná daoine óga? Ar 8 Nollaig, d'fhoilsigh nádúr Cell Biology torthaí comhfhoireann eolaithe na Síne chun cabhrú linn an cheist seo a fhreagairt.


"In layman's terms, the novel Coronavirus invasions age the lungs of older persons." Liu Guanghui, one of the paper's corresponding authors and a researcher at the Institute of Zoology, Chinese Academy of Sciences, told Science and Technology Daily that the results of the novel Coronavirus infection showed significantly accelerated aging of lung tissues.


Virus invasion, aging signs' spike '


Go cliniciúil, is é an phríomhchúis le bás in othair COVID-19 ná cliseadh riospráide mar gheall ar ghortú dian scamhóg.


What exactly has novel Coronavirus destroyed in the lungs? To clarify the situation, a joint research team from the Institute of Zoology of the Chinese Academy of Sciences, the First Affiliated Hospital of The Army Military Medical University and the Beijing Institute of Genomics of the Chinese Academy of Sciences conducted a detailed "cell-to-cell" and even "intracellular molecular" analysis of lung tissue from autopsy samples of elderly patients with COVID-19.


Trí phaiteolaíocht, próitéamaíocht agus ardteicnící traschuir cille singil a thréchur, rinne an fhoireann anailís ar shaintréithe paiteolaíocha 28 cineál éagsúil cille i gceithre mhórghrúpa cille, lena n-áirítear cealla epithelial scamhóg, cealla inotelial, cealla stromal agus cealla imdhíonachta.


"We found that lung cells in elderly patients showed more severe 'senility'." Some cell senescence markers, senescence related inflammatory factors and DNA oxidative damage markers were significantly upregulated, Liu said.


What are the outward manifestations of "aged" lung cells?


"We see apoptosis, shedding of lung epithelial cells." For example, liu said, there is also a reduction in cell-surface active substances, which normally support the normal dilation and contraction of the alveoli, and some basic respiratory functions of the alveoli are reduced.


Drooping, retardation, apoptosis, shedding... The performance of "old lung" was unusually prominent after the novel Coronavirus invasion.


Buaileann an timthriall, ag cur insult le díobháil


"The lung tissue of the elderly may be hit in a circular fashion by the virus." Liu Guanghui told Science and Technology Daily that there are already more Novel Coronavirus receptors (ACE2) on the lung cells of the elderly than the young, and the aging of the cells is more obvious after the virus invasions. In turn, cell aging further induces the upregulation of novel Coronavirus receptors, making the cells more vulnerable to virus attack. The age-mediated "gate opening" cycle repeats, introducing more viruses and accelerating lung failure.


Ina theannta sin, fuair an fhoireann carnadh mór de chealla idirthréimhseacha epithelial alveolar i samplaí fíocháin scamhóg COVID-19 bunaithe ar anailís bhithfhaisnéisíochta. Sna alveoli, tá cealla epithelial alveolar cineál I freagrach as malartú gáis, ach níl aon chumas athghiniúna acu agus is gá iad a athlánú trí dhifreáil cealla epithelial alveolar cineál II tar éis díobhála. Tugann flúirse na gceall idirthréimhseach sin le fios go bhfuil bac ar thacaíocht chineál ii.


The virus's entry into lung tissue also accelerated fibrosis, a form of lung aging, the study found. In combination with the human lung fibroblast model, we found that the silencing of longevity gene FOXO3 may promote the transformation of lung fibroblasts into myofibroblasts and mediate the occurrence of pulmonary fibrosis.


Tá an damáiste déanta níos measa ag na trí straitéis chun an geata a oscailt go leathan, tacaíocht a ghearradh amach, fiobróis cille a mhéadú, agus an víreas ag dul isteach i gcealla scamhóg daoine scothaosta.

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