Evidence map›Paper›PMID 34281194›Full record

ArticleInternational journal of molecular sciences2021

DRP1 Inhibition Rescues Mitochondrial Integrity and Excessive Apoptosis in CS-A Disease Cell Models.

Barbara Pascucci, Francesca Spadaro, Donatella Pietraforte, Chiara De Nuccio, Sergio Visentin, Paola Giglio, Eugenia Dogliotti, Mariarosaria D'Errico

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. AMPK/MFF Activation: Role in Mitochondrial Fission and Mitophagy in Dry Eye.Investigative ophthalmology & visual science · 2022
    Article
  6. 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

8 authors at 2 institutions in 1 country.

Barbara PascucciInstitute of Crystallography, Consiglio Nazionale delle Ricerche, 00015 Rome, Italy.ORCID 0000-0002-8383-8751
Francesca SpadaroCore Facilities, Istituto Superiore di Sanità, 00161 Rome, Italy.ORCID 0000-0002-6610-350X
Donatella PietraforteCore Facilities, Istituto Superiore di Sanità, 00161 Rome, Italy.ORCID 0000-0001-6370-912X
Chiara De NuccioResearch Coordination and Support Service, Istituto Superiore di Sanità, 00161 Rome, Italy.
Sergio VisentinNational Center for Research and Preclinical and Clinical Evaluation of Drugs, Istituto Superiore di Sanità, 00161 Rome, Italy.
Paola GiglioDepartment of Biology, Tor Vergata University, 00133 Rome, Italy.
Eugenia DogliottiDepartment of Environment and Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
Mariarosaria D'ErricoDepartment of Environment and Health, Istituto Superiore di Sanità, 00161 Rome, Italy.
Istituto Superiore di Sanità · ITUniversity of Rome Tor Vergata · IT

Funding

Ministero dell'Istruzione, dell'Università e della Ricerca 20152CB22L
6 · The paper itself

Abstract

Cockayne syndrome group A (CS-A) is a rare recessive progeroid disorder characterized by sun sensitivity and neurodevelopmental abnormalities. Cells derived from CS-A patients present as pathological hallmarks excessive oxidative stress, mitochondrial fragmentation and apoptosis associated with hyperactivation of the mitochondrial fission dynamin related protein 1 (DRP1). In this study, by using human cell models we further investigated the interplay between DRP1 and CSA and we determined whether pharmacological or genetic inhibition of DRP1 affects disease progression. Both reactive oxygen and nitrogen species are in excess in CS-A cells and when the mitochondrial translocation of DRP1 is inhibited a reduction of these species is observed together with a recovery of mitochondrial integrity and a significant decrease of apoptosis. This study indicates that the CSA-driven modulation of DRP1 pathway is key to control mitochondrial homeostasis and apoptosis and suggests DRP1 as a potential target in the treatment of CS patients.

Indexed as

AnimalsApoptosisCell LineCockayne SyndromeDisease ProgressionDynaminsHumansMicrotubule-Associated ProteinsMitochondriaMitochondrial DiseasesMitochondrial ProteinsModels, BiologicalOxidative StressQuinazolinonesReactive Oxygen SpeciesSignal Transduction3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneDNM1L protein, humanDynaminsMicrotubule-Associated ProteinsMitochondrial ProteinsQuinazolinonesReactive Oxygen Speciesapoptosiscockayne syndromeMDIVI-1mitochondrial dysfunction

Identifiers

PMID34281194
PMCPMC8268695
OpenAlexW3176723802

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.