Evidence map›Paper›PMID 34841263›Full record

ReviewMolecular biomedicine2021

Roles of host mitochondria in the development of COVID-19 pathology: Could mitochondria be a potential therapeutic target?

Kavya Srinivasan, Ashutosh Kumar Pandey, Ashlena Livingston, Sundararajan Venkatesh

Abstract readReview
In one paragraph

Review in Molecular biomedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

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  12. SIRT3 Is a Critical Regulator of Mitochondrial Function of Fibroblasts in Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2023
    Article
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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

4 authors.

Kavya SrinivasanDepartment of Microbiology, Biochemistry and Molecular Genetics, Rutgers -New Jersey Medical School, The State University of New Jersey, Newark, NJ USA.
Ashutosh Kumar PandeyDepartment of Pharmacology, Physiology and Neuroscience, Rutgers -New Jersey Medical School, The State University of New Jersey, Newark, NJ USA.
Ashlena LivingstonDallas Baptist University, Dallas, TX United States.
Sundararajan VenkateshDepartment of Microbiology, Biochemistry and Molecular Genetics, Rutgers -New Jersey Medical School, The State University of New Jersey, Newark, NJ USA.

Funding

American Heart Association 20CDA35260096American Heart Association 20TPA3542000
6 · The paper itself

Abstract

The recent emergence of severe acute respiratory syndrome-Corona Virus 2 (SARS-CoV-2) in late 2019 and its spread worldwide caused an acute pandemic of Coronavirus disease 19 (COVID-19). Since then, COVID-19 has been under intense scrutiny as its outbreak led to significant changes in healthcare, social activities, and economic settings worldwide. Although angiotensin-converting enzyme-2 (ACE-2) receptor is shown to be the primary port of SARS-CoV-2 entry in cells, the mechanisms behind the establishment and pathologies of COVID-19 are poorly understood. As recent studies have shown that host mitochondria play an essential role in virus-mediated innate immune response, pathologies, and infection, in this review, we will discuss in detail the entry and progression of SARS-CoV-2 and how mitochondria could play roles in COVID-19 disease. We will also review the potential interactions between SARS-CoV-2 and mitochondria and discuss possible treatments, including whether mitochondria as a potential therapeutic target in COVID-19. Understanding SARS-CoV-2 and mitochondrial interactions mediated virus establishment, inflammation, and other consequences may provide a unique mechanism and conceptual advancement in finding a novel treatment for COVID-19.

Indexed as

ACE-2 receptorCOVID-19Cytokine stormInflammationMitochondriaSARS-CoV-2

Identifiers

PMID34841263
PMCPMC8608434

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.