Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText.
Kick-your-searchterm to multiple Engines kick-your-query now !>
A dictionary by aggregated review articles of nephrology, medicine and the life sciences
Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

suck abstract from ncbi


10.1016/j.gene.2021.146069

http://scihub22266oqcxt.onion/10.1016/j.gene.2021.146069
suck pdf from google scholar
34848322!8634871!34848322
unlimited free pdf from europmc34848322    free
PDF from PMC    free
html from PMC    free
PDF vom PMID34848322  :  Publisher

suck abstract from ncbi

pmid34848322
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Understanding the role of telomere attrition and epigenetic signatures in COVID-19 severity #MMPMID34848322
  • Mahmoodpoor A; Sanaie S; Roudbari F; Sabzevari T; Sohrabifar N; Kazeminasab S
  • Gene 2022[Feb]; 811 (ä): 146069 PMID34848322show ga
  • 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.
  • |*Epigenesis, Genetic[MESH]
  • |*Epigenomics[MESH]
  • |*Severity of Illness Index[MESH]
  • |COVID-19/*genetics/*immunology/*metabolism/virology[MESH]
  • |DNA Methylation[MESH]
  • |Genetic Predisposition to Disease[MESH]
  • |Humans[MESH]
  • |Immunity[MESH]
  • |MicroRNAs/metabolism[MESH]
  • |SARS-CoV-2/immunology[MESH]
  • |Telomere/*genetics[MESH]


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    146069 ä.811 2022