Evidence map›Paper›PMID 32905655›Full record

ReviewJournal of biochemical and molecular toxicology2021

Susceptibility to COVID-19 in populations with health disparities: Posited involvement of mitochondrial disorder, socioeconomic stress, and pollutants.

Yunyi Yao, David A Lawrence

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of biochemical and molecular toxicology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. COVID-19 and the Assessment of Coenzyme Q10.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  8. Social characterization of COVID-19 in the state of Amazonas, Brazil.American journal of translational research · 2022
    Article
  9. Review
  10. The Role of Immunogenetics in COVID-19.International journal of molecular sciences · 2021
    Review
  11. 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

2 authors at 1 institution in 1 country.

Yunyi YaoWadsworth Center, New York State Department of Health, Center for Medical Science, Albany, New York.ORCID http://orcid.org/0000-0002-6522-8095
David A LawrenceWadsworth Center, New York State Department of Health, Center for Medical Science, Albany, New York.ORCID http://orcid.org/0000-0002-8940-9640
New York State Department of Health · US

Funding

Prenatal environmental toxicants induce neuroinflammation causing autistic behaviorsR01ES025584 · NIEHS · WADSWORTH CENTER · PI LAWRENCE, DAVID A · 2016 to 2020
$2.9M
NIEHS NIH HHS R01 ES025584NIH HHS ES025584
6 · The paper itself

Abstract

SARS-CoV-2 is a novel betacoronavirus that has caused the global health crisis known as COVID-19. The implications of mitochondrial dysfunction with COVID-19 are discussed as well as deregulated mitochondria and inter-organelle functions as a posited comorbidity enhancing detrimental outcomes. Many environmental chemicals (ECs) and endocrine-disrupting chemicals can do damage to mitochondria and cause mitochondrial dysfunction. During infection, SARS-CoV-2 via its binding target ACE2 and TMPRSS2 can disrupt mitochondrial function. Viral genomic RNA and structural proteins may also affect the normal function of the mitochondria-endoplasmic reticulum-Golgi apparatus. Drugs considered for treatment of COVID-19 should consider effects on organelles including mitochondria functions. Mitochondrial self-balance and clearance via mitophagy are important in SARS-CoV-2 infection, which indicate monitoring and protection of mitochondria against SARS-CoV-2 are important. Mitochondrial metabolomic analysis may provide new indicators of COVID-19 prognosis. A better understanding of the role of mitochondria during SARS-CoV-2 infection may help to improve intervention therapies and better protect mitochondrial disease patients from pathogens as well as people living with poor nutrition and elevated levels of socioeconomic stress and ECs.

Indexed as

COVID-19Mitochondrial DiseasesAngiotensin-Converting Enzyme 2Environmental PollutantsHumansSARS-CoV-2Serine EndopeptidasesSocioeconomic FactorsACE2 protein, humanAngiotensin-Converting Enzyme 2Environmental PollutantsSerine EndopeptidasesTMPRSS2 protein, humandysfunctionexposomeimmunosenescencemetabolomicsmitochondriapollutantSARS-CoV-2socioeconomicstress

Identifiers

PMID32905655
PMCPMC9340490
OpenAlexW3086799986

What OpenQuestion holds

Textmetadata
LicenceTDM
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.