Evidence map›Paper›PMID 33662449›Full record

ReviewPharmacology & therapeutics2021

SARS-CoV-2 and other coronaviruses negatively influence mitochondrial quality control: beneficial effects of melatonin.

Saeed Mehrzadi, Mohammad Yahya Karimi, Alireza Fatemi, Russel J Reiter, Azam Hosseinzadeh

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
7.8field-weighted citation impact, top 1% 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

43 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
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  7. Revealing Cell-Free Mitochondrial DNA Breakage Patterns as Novel Biomarkers for Sepsis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Article
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  11. The Essential Role of Mitochondrial Dynamics in Viral Infections.International journal of molecular sciences · 2025
    Review
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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

5 authors at 3 institutions in 2 countries.

Saeed MehrzadiRazi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
Mohammad Yahya KarimiRazi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.
Alireza FatemiFunctional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Russel J ReiterDepartment of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA.
Azam HosseinzadehRazi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran. Electronic address: hoseinzadeh.a@iums.ac.ir.
Iran University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronaviruses (CoVs) are a group of single stranded RNA viruses, of which some of them such as SARS-CoV, MERS-CoV, and SARS-CoV-2 are associated with deadly worldwide human diseases. Coronavirus disease-2019 (COVID-19), a condition caused by SARS-CoV-2, results in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) associated with high mortality in the elderly and in people with underlying comorbidities. Results from several studies suggest that CoVs localize in mitochondria and interact with mitochondrial protein translocation machinery to target their encoded products to mitochondria. Coronaviruses encode a number of proteins; this process is essential for viral replication through inhibiting degradation of viral proteins and host misfolded proteins including those in mitochondria. These viruses seem to maintain their replication by altering mitochondrial dynamics and targeting mitochondrial-associated antiviral signaling (MAVS), allowing them to evade host innate immunity. Coronaviruses infections such as COVID-19 are more severe in aging patients. Since endogenous melatonin levels are often dramatically reduced in the aged and because it is a potent anti-inflammatory agent, melatonin has been proposed to be useful in CoVs infections by altering proteasomal and mitochondrial activities. Melatonin inhibits mitochondrial fission due to its antioxidant and inhibitory effects on cytosolic calcium overload. The collective data suggests that melatonin may mediate mitochondrial adaptations through regulating both mitochondrial dynamics and biogenesis. We propose that melatonin may inhibit SARS-CoV-2-induced cell damage by regulating mitochondrial physiology.

Indexed as

COVID-19 Drug TreatmentAgedAnimalsAntioxidantsCoronavirus InfectionsCOVID-19FemaleHumansMelatoninMitochondriaSevere Acute Respiratory SyndromeVirus ReplicationAntioxidantsMelatoninApoptosisAutophagyChaperone proteinsCoronavirusesCOVID-19FissionFusionMelatoninMitochondrial dynamics

Identifiers

PMID33662449
PMCPMC7919585
OpenAlexW3135193588

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.