Evidence map›Paper›PMID 34513032›Full record

ArticleSovremennye tekhnologii v meditsine2020

A New Cofilin-Dependent Mechanism for the Regulation of Brain Mitochondria Biogenesis and Degradation.

T F Kovaleva, N S Maksimova, P V Pchelin, V I Pershin, N M Tkachenko, M R Gainullin, I V Mukhina

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Sovremennye tekhnologii v meditsine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 98% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Cofilin(s) and Mitochondria: Function Beyond Actin Dynamics.International journal of molecular sciences · 2025
    Review
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

7 authors at 2 institutions in 2 countries.

T F KovalevaSenior Researcher, Molecular and Cellular Technologies Department, Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia.
N S MaksimovaPhD Student, Junior Researcher, Molecular and Cellular Technologies Department, Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia.
P V PchelinLaboratory Assistant, Molecular and Cellular Technologies Department, Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia.
V I PershinLaboratory Assistant, Molecular and Cellular Technologies Department, Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia.
N M TkachenkoJunior Researcher, Molecular and Cellular Technologies Department, Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia.
M R GainullinSenior Researcher, Molecular and Cellular Technologies Department, Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia, Researcher, Norwegian PSC Research Center, Department of Transplantation Medicine, Division of Surgery, Inflammatory Diseases and Transplantation, Oslo University Hospital Rikshospitalet, P.O. Box 4950, Nydalen, Oslo, 0424, Norway, Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, P.O. Box 1171, Blindern, Oslo, 0318, Norway.
I V MukhinaProfessor, Director of the Institute of Fundamental Medicine, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia, Head of the Department of Normal Physiology named after N.Y. Belenkov, Privolzhsky Research Medical University, 10/1 Minin and Pozharsky Square, Nizhny Novgorod, 603005, Russia, Professor, Department of Neurotechnologies, Institute of Biology and Biomedicine, National Research Lobachevsky State University of Nizhni Novgorod, 23 Prospekt Gagarina, Nizhny Novgorod, 603950, Russia.
Privolzhsky Research Medical University · RUOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MATERIALS AND

methodsThe experiments were performed with C57BL/6 mice. To obtain cytoplasmic and mitochondrial fractions of the brain tissue, differential centrifugation was used. Expressions of cofilin, phospho-cofilin, K48- and K63-associated chains of ubiquitin, and the autophagy marker LC3B were determined using electrophoresis, immunoprecipitation and Western blot methods. To study the processes of ubiquitination, we used PR619 - the inhibitor of deubiquitinating enzymes. Respiratory activity of brain mitochondria was evaluated using high-resolution fluorespirometry.

resultsModification of cofilin by non-canonical K63 multiubiquitin chains in the cytoplasm and mitochondria from murine brain was demonstrated. Different levels of phospho-cofilin, cofilin, and its ubiquitinated proteoforms were found. PR619, the inhibitor of deubiquitinating enzymes, affects the expression of phosphorylated and ubiquitinated forms of cofilin in the mitochondria and cytoplasm, at the same time it changes the activity of tissue respiration and mitophagy.

conclusionThe sensitivity of cofilin to the inhibitor of deubiquitinating enzymes indicates the existence of a new non-catabolic mechanism of cofilin modification, which may be involved in the regulation of mitochondrial functions, specifically, the mitochondrial respiration and autophagy. The data help understand the molecular mechanisms of mitochondrial function in normal and pathological conditions, which may be useful in developing novel methods for the treatment of diseases of the nervous system.

Indexed as

autophagycofilindeubiquitinating enzymesmitochondriaPR619ubiquitin

Identifiers

PMID34513032
PMCPMC8353704
OpenAlexW3010280425

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.