Publication date: Jul 17, 2025
Elderly individuals were disproportionally affected during the COVID-19 pandemic, and more than 80% of the global COVID-19-related deaths between 2020 and 2021 occurred among people aged 60 years or older. Several cellular modifications in aged cells may lead to systemic inflammation and fibrotic responses. Age or exogenous insults induce cellular senescence, further increasing the release of pro-inflammatory mediators, leading to the condition known as inflammaging, that can contribute to disease severity. Older individuals presented signs of systemic hyperinflammation in severe COVID-19, but few studies analyzed the influence of age on lung tissue responses in cases of severe COVID-19. We hypothesized that age related alterations regarding innate/acquired immunity and cellular senescence in lung tissue of individuals without lung diseases could predispose to viral infection. We also aimed to identify how the aged lung responded to severe COVID-19 infection. We studied lung tissues from 19 individuals that died from non-pulmonary causes and 28 adult individuals who died from COVID-19 between March and May of 2020, divided according to their age (> or
| Concepts | Keywords |
|---|---|
| Elderly | Autopsy |
| Pandemic | COVID-19 |
| Pulmonary | Immunopathology |
| Viral | Lung inflammation |
| Senescence |
Semantics
| Type | Source | Name |
|---|---|---|
| disease | MESH | COVID-19 |
| disease | MESH | inflammation |
| pathway | REACTOME | Cellular Senescence |
| pathway | REACTOME | Release |
| disease | MESH | lung diseases |
| disease | MESH | viral infection |
| disease | MESH | infection |
| disease | MESH | causes |
| disease | MESH | Long Covid |
| disease | MESH | Lung inflammation |