Evidence map›Paper›PMID 34848322›Full record

ReviewGene2022

Understanding the role of telomere attrition and epigenetic signatures in COVID-19 severity.

Ata Mahmoodpoor, Sarvin Sanaie, Faranak Roudbari, Tara Sabzevari, Nasim Sohrabifar, Somayeh Kazeminasab

Open access · greenAbstract readReview
In one paragraph

Review in Gene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The impact of COVID-19 on "biological aging".Frontiers in immunology · 2024
    Review
  6. Article
  7. SARS-CoV-2 and the DNA damage response.The Journal of general virology · 2023
    Review
  8. Review
  9. Review
  10. Association between leukocyte telomere length and COVID-19 severity.The Egyptian journal of medical human genetics · 2023
    Article
  11. Article
  12. A cautionary note on altered pace of aging in the COVID-19 era.Forensic science international. Genetics · 2022
    Article
  13. Article
  14. Article
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

6 authors at 3 institutions in 1 country.

Ata MahmoodpoorImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Sarvin SanaieNeurosciences Research center, Aging Research Institute, Tabriz University of Medical Sciences, Tabriz, Iran.
Faranak RoudbariTabriz University, Faculty of Natural Sciences, Tabriz, Iran.
Tara SabzevariStudent Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Nasim SohrabifarCardiovascular Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Somayeh KazeminasabDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran; Research Vice-Chancellor, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran. Electronic address: somayyekazeminasab@yahoo.com.
Tabriz University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRUniversity of Tabriz · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Within the past several decades, the emergence and spread of infectious diseases with pandemic potential have endangered human lives. Coronavirus disease 2019 (COVID-19) outbreak represents an unprecedented threat for all health systems worldwide. The clinical spectrum of COVID-19 is highly heterogeneous, ranging from asymptomatic and mild upper respiratory tract illness to severe interstitial pneumonia with respiratory failure and even death. Highly age-dependent patterns of immune response potentially explain the higher rates of the severe forms of COVID-19 in elderly patients. However, genetic and epigenetic architecture can influence multiple biological processes during the lifespan, therefore as far as our knowledge shows, vulnerability to viral infection concerning telomere length and epigenetic signature is not a new idea. This review aims is to summarize the current understanding of the role of telomere length and epigenetic mechanisms on the severity of COVID-19. The current knowledge highlights the significant association between the shorter telomere length and the higher risk of developing severe COVID-19. Differential DNA methylation patterns and miRNA expression profiles imply that these hallmarks can play a pivotal role in COVID- 19 pathogenesis. Understanding the causes of inter-individual variations in COVID-19 outcomes could provide clues to the development of the personalized therapeutic intervention.

Indexed as

Epigenesis, GeneticEpigenomicsSeverity of Illness IndexCOVID-19DNA MethylationGenetic Predisposition to DiseaseHumansImmunityMicroRNAsSARS-CoV-2TelomereMicroRNAsCOVID-19EpigeneticSARS-CoV-2SeverityTelomere

Identifiers

PMID34848322
PMCPMC8634871
OpenAlexW3214741708

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.