‘Unusual’ form of cell death underlies lung damage in COVID-19 patients: Study

The study analysed human tissues and collected autopsies of patients who died of respiratory failure caused by COVID infection


Published May 21, 2024 | 12:51 AM Updated May 21, 2024 | 12:51 AM

Lung damage in COVID patients (Wikimedia Commons)

An unusual form of cell death could lead to a COVID patient’s lungs suffering extreme damage, potentially resulting in life-threatening conditions such as inflammation and acute respiratory disorders, according to a new study.

The ability to inhibit this unusual form of cell death – ferroptosis – can offer doctors new ways of treating COVID lung disease, the research suggested.

Cell death, where a cell stops functioning, can be natural or could result from causes such as a disease or an injury. The most common form of cell death involves cells “chopping up” the molecules inside, researchers explained, adding that this occurs in humans, both when they are ill or are ageing.

However, in ferroptosis, the relatively uncommon form of cell death, cells die because their outer fat layers collapse, the researchers at Columbia University in the US said.

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Findings from Columbia University’s study

In this study, they analysed human tissues and collected autopsies of patients who died of respiratory failure caused by COVID infection. Samples from hamsters were also analysed.

The team found that most cells were dying through the ferroptosis mechanism, forming the underlying basis for lung disease in Coronavirus patients.

Therefore, drugs that target and prevent the ferroptosis form of cell death could help improve the treatment course for COVID, the researchers said.

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“This finding adds crucial insight to our understanding of how COVID-19 affects the body and it will significantly improve our ability to fight life-threatening cases of the disease,” said Brent Stockwell, chair of the Department of Biological Sciences at Columbia, and co-lead author of the study published in the journal Nature Communications.

Previous studies have shown that ferroptosis, while instrumental to certain normal bodily processes, can also attack and kill healthy cells in patients with neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease.

The authors said that the ability to inhibit ferroptosis could offer doctors new ways of combating cell death that should not be occurring, as in the case of COVID-19 lung disease.

“We’re hopeful that these important new findings could improve our ability to confront this pernicious disease, which, in too many cases, still diminishes health outcomes and results in death,” said Stockwell.

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