Evidence map›Paper›PMID 38017502›Full record

ArticleClinical epigenetics2023

Epigenetic age acceleration in surviving versus deceased COVID-19 patients with acute respiratory distress syndrome following hospitalization.

Yosra Bejaoui, Fathima Humaira Amanullah, Mohamad Saad, Sara Taleb, Martina Bradic, Andre Megarbane, Ali Ait Hssain, Charbel Abi Khalil, Nady El Hajj

Abstract read
In one paragraph

Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

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  15. The impact of COVID-19 on "biological aging".Frontiers in immunology · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Yosra BejaouiCollege of Health and Life Sciences, Hamad Bin Khalifa University, Qatar Foundation, Education City, Doha, Qatar.
Fathima Humaira AmanullahCollege of Health and Life Sciences, Hamad Bin Khalifa University, Qatar Foundation, Education City, Doha, Qatar.
Mohamad SaadQatar Computing Research Institute, Hamad Bin Khalifa University, Qatar Foundation, Doha, Qatar.
Sara TalebCollege of Health and Life Sciences, Hamad Bin Khalifa University, Qatar Foundation, Education City, Doha, Qatar.
Martina BradicDepartment of Genetic Medicine, Weill Cornell Medicine, New York, USA.
Andre MegarbaneGilbert and Rose-Mary Chagoury School of Medicine, Lebanese American Univeristy, Beirut, Lebanon.
Ali Ait HssainMedical Intensive Care Unit, Hamad Medical Corporation, Doha, Qatar.
Charbel Abi Khalil *Department of Genetic Medicine, Weill Cornell Medicine, New York, USA. cha2022@med.cornell.edu.
Nady El HajjCollege of Health and Life Sciences, Hamad Bin Khalifa University, Qatar Foundation, Education City, Doha, Qatar. nelhajj@hbku.edu.qa.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

backgroundAging has been reported as a major risk factor for severe symptoms and higher mortality rates in COVID-19 patients. Molecular hallmarks such as epigenetic alterations and telomere attenuation reflect the biological process of aging. Epigenetic clocks have been shown to be valuable tools for measuring biological age in various tissues and samples. As such, these epigenetic clocks can determine accelerated biological aging and time-to-mortality across various tissues. Previous reports have shown accelerated biological aging and telomere attrition acceleration following SARS-CoV-2 infection. However, the effect of accelerated epigenetic aging on outcome (death/recovery) in COVID-19 patients with acute respiratory distress syndrome (ARDS) has not been well investigated.

resultsIn this study, we measured DNA methylation age and telomere attrition in 87 severe COVID-19 cases with ARDS under mechanical ventilation. Furthermore, we compared dynamic changes in epigenetic aging across multiple time points until recovery or death. Epigenetic age was measured using the Horvath, Hannum, DNAm skin and blood, GrimAge, and PhenoAge clocks, whereas telomere length was calculated using the surrogate marker DNAmTL. Our analysis revealed significant accelerated epigenetic aging but no telomere attrition acceleration in severe COVID-19 cases. In addition, we observed epigenetic age deceleration at inclusion versus end of follow-up in recovered but not in deceased COVID-19 cases using certain clocks. When comparing dynamic changes in epigenetic age acceleration (EAA), we detected higher EAA using both the Horvath and PhenoAge clocks in deceased versus recovered patients. The DNAmTL measurements revealed telomere attrition acceleration in deceased COVID-19 patients between inclusion and end of follow-up and a significant change in dynamic telomere attrition acceleration when comparing patients who recovered versus those who died.

conclusionsEAA and telomere attrition acceleration were associated with treatment outcomes in hospitalized COVID-19 patients with ARDS. A better understanding of the long-term effects of EAA in COVID-19 patients and how they might contribute to long COVID symptoms in recovered individuals is urgently needed.

Indexed as

COVID-19Respiratory Distress SyndromeAccelerationDNA MethylationEpigenesis, GeneticHospitalizationHumansPost-Acute COVID-19 SyndromeSARS-CoV-2COVID-19Epigenetic age accelerationEpigenetic clocksSARS-CoV-2

Identifiers

PMID38017502
PMCPMC10685564

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.