◎ Science and Technology Daily reporter Zhang Jiaxing
Authoritative data show that the average age of covid-19 deaths worldwide is more than 70 years old!
Why are the elderly more likely to die than young people after contracting the new crown virus? On December 8, Nature cell biology published the results of a joint team of Chinese scientists to help us answer this question.
"In layman's terms, the invasion of the new crown virus has made the lungs of the elderly older." Liu Guanghui, one of the corresponding authors of the paper and a researcher at the Institute of Zoology of the Chinese Academy of Sciences, told Science and Technology Daily that the results of the study showed that the lung tissue infected by the new crown virus showed significant accelerated aging.
Viral invasion, aging indications "steep rise"
Clinically, the main cause of death in patients with covid-19 is respiratory failure due to severe lung injury.
What exactly has COVID-19 destroyed in the lungs? In order to clarify the situation, the joint research team of 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 analysis of the lung tissue of the autopsy samples of elderly patients with new crown and even "cell by cell".
Combining techniques such as pathology, proteome and high-throughput single-cell nuclear transcriptome, the research team analyzed the pathological characteristics of 28 different cell types, including four major cell classes of lung epithelial cells, endothelial cells, stromal cells and immune cells.
"We found that the lung tissue cells of elderly COVID-19 patients showed a more severe 'aging state'." Liu Guanghui said that some cellular aging markers, aging-related inflammatory factors, DNA oxidative damage markers, etc. have been significantly upregulated.
What are the external manifestations of "aging" lung cells?
"We see apoptosis and shedding of lung epithelial cells." For example, Liu Guanghui said, there is also a reduction in cellular surfactants, which originally support the normal relaxation and contraction of alveoli, and some of the basic respiratory functions of the alveoli are degraded after the reduction.
Slowness, withering, shedding... After the invasion of the new crown virus, the performance of "old lungs" was unusually prominent.
Aging, shedding of epithelial cells, elevated apoptosis, excessive inflammatory response, increased coagulation and fibrosis are the main pathological phenotypic features of the lungs of patients with new coronary pneumonia, and also the "birthplace" of systemic immune damage throughout the body.
Circular blows, worse
"The lung tissue of the elderly may be hit by the circulation of the virus." Liu Guanghui told the Science and Technology Daily reporter that the new coronavirus receptor (ACE2) on the lung cells of the elderly is originally more than that of young people, and the aging is more obvious after the virus invades the cell, and the cell aging in turn further induces the upregulation of the new crown virus receptor, and the cells are more likely to be attacked by the virus. Aging-mediated "great openings" cycle back and forth, introducing more viruses and accelerating the onset of lung failure.
In addition, based on bioinformatics analysis, the team also found that a large number of alveolar epithelial transition cells have accumulated in the new crown pneumonia lung tissue samples. In the alveoli, alveolar epithelial cells type I are responsible for gas exchange, but they do not have regenerative capacity and need to be differentiated and supplemented by type II alveolar epithelial cells after injury. The presence of a large number of such transitional cells suggests that the "support" of type II is blocked.
Studies have found that the virus entering lung tissue also accelerates the fibrosis of the lungs (a manifestation of lung aging). Combined with a research model of human lung fibroblasts, the researchers found that the silencing of the longevity gene FOXO3 may have facilitated the transformation of fibroblasts into myofibroblasts in the lungs, mediating the occurrence of pulmonary fibrosis.
The three major strategies of opening the "city gate", cutting off the "support", intensifying cell fibrosis, and entering the lung cells of the elderly have made the blow to the elderly "worse".
New associations between aging and infection
"We found a significant association between aging and COVID-19 infection." Liu Guanghui said that in addition to the lungs, other organs may also accelerate "aging" after being attacked by the virus, and follow-up research is being carried out.
These scientific studies have innovatively linked the aging mechanism to the infection of the new crown virus, bringing a new perspective to human understanding the pathogenesis of the new crown virus.
The study systematically analyzed the disease changes of various cell types in the lung tissue of new crown patients, and identified the accelerated aging phenotype of the lungs of new crown pneumonia patients for the first time, which provided a possible explanation for the increase in the mortality rate of the elderly caused by the new crown virus infection and the prognosis of various sequelae.
"Analyzing the accelerated aging of the lungs is a key pathology, it can further guide the intervention of new crown pneumonia." Some mature aging intervention strategies may be potential prevention and treatment methods to alleviate organ damage from COVID-19. Liu Guanghui said that for example, the previous team's research found that vitamin C, which has the effect of delaying cellular aging, can inhibit the expression of new coronavirus receptor proteins, which may improve the resistance of the elderly to the new crown virus.
According to reports, the research was completed by the team of academician Bian Xiuwu of the First Affiliated Hospital (Southwest Hospital) of the Army Military Medical University (Third Military Medical University), the Liu Guanghui Research Group and Qu Jing Research Group of the Institute of Zoology of the Chinese Academy of Sciences, and the Zhang Weiqi Research Group of the Beijing Institute of Genomics of the Chinese Academy of Sciences, and was funded by the Ministry of Science and Technology, the National Natural Science Foundation of China, the Chinese Academy of Sciences and the Beijing MunicipalIty.
Source: Science and Technology Daily
Editor: Zhang Shuang
Review: Wang Xiaolong
Final Judge: Liu Haiying