Evidence map›Paper›PMID 34085316›Full record

ArticleJournal of pineal research2021

Melatonin reshapes the mitochondrial network and promotes intercellular mitochondrial transfer via tunneling nanotubes after ischemic-like injury in hippocampal HT22 cells.

Maria Gemma Nasoni, Silvia Carloni, Barbara Canonico, Sabrina Burattini, Erica Cesarini, Stefano Papa, Marica Pagliarini, Patrizia Ambrogini, Walter Balduini, Francesca Luchetti

Open access · hybridAbstract read
In one paragraph

Article in Journal of pineal research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

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14 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

Maria Gemma NasoniDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Silvia CarloniDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.ORCID https://orcid.org/0000-0003-3634-3454
Barbara CanonicoDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Sabrina BurattiniDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Erica CesariniDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Stefano PapaDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Marica PagliariniDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Patrizia AmbroginiDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Walter BalduiniDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.ORCID https://orcid.org/0000-0001-8438-9559
Francesca LuchettiDepartment of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.ORCID https://orcid.org/0000-0002-8225-3129
University of Urbino · IT

Funding

Università degli Studi di Urbino Carlo Bo
6 · The paper itself

Abstract

Mitochondrial dysfunction is considered one of the hallmarks of ischemia/reperfusion injury. Mitochondria are plastic organelles that undergo continuous biogenesis, fusion, and fission. They can be transferred between cells through tunneling nanotubes (TNTs), dynamic structures that allow the exchange of proteins, soluble molecules, and organelles. Maintaining mitochondrial dynamics is crucial to cell function and survival. The present study aimed to assess the effects of melatonin on mitochondrial dynamics, TNT formation, and mitochondria transfer in HT22 cells exposed to oxygen/glucose deprivation followed by reoxygenation (OGD/R). The results showed that melatonin treatment during the reoxygenation phase reduced mitochondrial reactive oxygen species (ROS) production, improved cell viability, and increased the expression of PGC1α and SIRT3. Melatonin also preserved the expression of the membrane translocase proteins TOM20 and TIM23, and of the matrix protein HSP60, which are involved in mitochondrial biogenesis. Moreover, it promoted mitochondrial fusion and enhanced the expression of MFN2 and OPA1. Remarkably, melatonin also fostered mitochondrial transfer between injured HT22 cells through TNT connections. These results provide new insights into the effect of melatonin on mitochondrial network reshaping and cell survival. Fostering TNTs formation represents a novel mechanism mediating the protective effect of melatonin in ischemia/reperfusion injury.

Indexed as

AnimalsBrain IschemiaCell LineCell Membrane StructuresHippocampusMelatoninMiceMitochondriaNanotubesNeuronsReperfusion InjuryMelatoninTunneling NanotubesHT22melatoninmitochondrial networkoxygen-glucose deprivationtunneling nanotubes

Identifiers

PMID34085316
PMCPMC8365755
OpenAlexW3165578448

What OpenQuestion holds

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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.