Evidence map›Paper›PMID 32850106›Full record

ArticleTherapeutic advances in chronic disease2020

Teriflunomide preserves peripheral nerve mitochondria from oxidative stress-mediated alterations.

Bimala Malla, Samuel Cotten, Rebecca Ulshoefer, Friedemann Paul, Anja E Hauser, Raluca Niesner, Helena Bros, Carmen Infante-Duarte

Open access · goldAbstract read
In one paragraph

Article in Therapeutic advances in chronic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Bimala MallaCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Institute for Medical Immunology, Berlin, Germany.
Samuel CottenCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Institute for Medical Immunology, Berlin, Germany.
Rebecca UlshoeferCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Institute for Medical Immunology, Berlin, Germany.
Friedemann PaulNeuroCure Clinical Research Center, Charité - Universitätsmedizin Berlin and Experimental & Clinical Research Center (ECRC), Max Delbrueck Center (MDC) for Molecular Medicine, Berlin, Germany and Charité - Universitätsmedizin Berlin, Berlin, Germany.
Anja E HauserMedizinische Klinik mit Schwerpunkt Rheumatologie und Klinische Immunologie, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt - Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany Deutsches Rheuma-Forschungszentrum, Berlin, Germany.
Raluca NiesnerDynamic and Functional in vivo Imaging, Deutsches Rheuma-Forschungszentrum, Berlin, Germany and Veterinary Medicine, Freie Universität Berlin, Germany.
Helena BrosCharité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin and Berlin Institute of Health, Institute for Medical Immunology, Berlin, Germany.
Carmen Infante-DuarteInstitute for Medical Immunology, Charité - Universitätsmedizin Berlin and Experimental & Clinical Research Center (ECRC), MDC for Molecular Medicine and Charité - Universitätsmedizin, Campus Virchow Klinikum, Augustenburger Platz 1, Berlin 13353, Germany.ORCID https://orcid.org/0000-0003-3005-351X
Humboldt-Universität zu Berlin · DECharité - Universitätsmedizin Berlin · DEGerman Rheumatism Research Centre · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction is a common pathological hallmark in various inflammatory and degenerative diseases of the central nervous system, including multiple sclerosis (MS). We previously showed that oxidative stress alters axonal mitochondria, limiting their transport and inducing conformational changes that lead to axonal damage. Teriflunomide (TFN), an oral immunomodulatory drug approved for the treatment of relapsing forms of MS, reversibly inhibits dihydroorotate dehydrogenase (DHODH). DHODH is crucial for

Indexed as

dihydroorotate dehydrogenase (DHODH)mitochondriamitochondrial dynamicsneurodegenerationoxidative stressteriflunomide (TFN)

Identifiers

PMID32850106
PMCPMC7425321
OpenAlexW3048739314

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.